bts/ics guideline for the ventilatory management of acute

BTS/ICS guideline for the ventilatory managementof acute hypercapnic respiratory failure in adultsA Craig Davidson,1 Stephen Banham,1 Mark Elliott,2 Daniel Kennedy,3 Colin Gelder,4

Alastair Glossop,5 Alistair Colin Church,6 Ben Creagh-Brown,7 James William Dodd,8,9

Tim Felton,10 Bernard Foëx,11 Leigh Mansfield,12 Lynn McDonnell,13 Robert Parker,14

Caroline Marie Patterson,15 Milind Sovani,16 Lynn Thomas,17 BTS Standards ofCare Committee Member, British Thoracic Society/Intensive Care Society AcuteHypercapnic Respiratory Failure Guideline Development Group, On behalf of theBritish Thoracic Society Standards of Care Committee

▸ Additional material ispublished online only. To viewplease visit the journal online(http://dx.doi.org/10.1136/thoraxjnl-2015-208209).

For numbered affiliations seeend of article.

Correspondence toDr A C Davidson,BTS, 17 Doughty Street,London WC1N 2PL, UK;[email protected]

Healthcare providers need touse clinical judgement,knowledge and expertise whendeciding whether it isappropriate to applyrecommendations for themanagement of patients. Therecommendations cited hereare a guide and may not beappropriate for use in allsituations. The guidanceprovided does not override theresponsibility of healthcareprofessionals to make decisionsappropriate to thecircumstances of each patient,in consultation with the patientand/or their guardian or carer.

Received 17 December 2015Accepted 10 January 2016

▸ http://dx.doi.org/10.1136/thoraxjnl-2016-208281

To cite: Davidson AC,Banham S, Elliott M, et al.Thorax 2016;71:ii1–ii35.

SUMMARY OF RECOMMENDATIONSPrinciples of mechanical ventilationModes of mechanical ventilationRecommendation1. Pressure-targeted ventilators are the devices ofchoice for acute NIV (Grade B).Good practice points▸ Both pressure support (PS) and pressure control

modes are effective.▸ Only ventilators designed specifically to deliver

NIV should be used.

Choice of interface for NIVRecommendation2. A full face mask (FFM) should usually be thefirst type of interface used (Grade D).Good practice points▸ A range of masks and sizes is required and staff

involved in delivering NIV need training in andexperience of using them.

▸ NIV circuits must allow adequate clearance ofexhaled air through an exhalation valve or anintegral exhalation port on the mask.

Indications for and contra-indications to NIV inAHRFRecommendation3. The presence of adverse features increase therisk of NIV failure and should prompt consider-ation of placement in high dependency unit(HDU)/intensive care unit (ICU) (Grade C).Good practice points▸ Adverse features should not, on their own, lead

to withholding a trial of NIV.▸ The presence of relative contra-indications

necessitates a higher level of supervision, consid-eration of placement in HDU/ICU and an earlyappraisal of whether to continue NIV or toconvert to invasive mechanical ventilation(IMV).

Monitoring during NIVGood practice points▸ Oxygen saturation should be continuously

monitored.▸ Intermittent measurement of pCO2 and pH is

required.

▸ ECG monitoring is advised if the patient has apulse rate >120 bpm or if there is dysrhythmiaor possible cardiomyopathy.

Supplemental oxygen therapy with NIVRecommendations4. Oxygen enrichment should be adjusted toachieve SaO2 88–92% in all causes of acute hyper-capnic respiratory failure (AHRF) treated by NIV(Grade A).5. Oxygen should be entrained as close to thepatient as possible (Grade C).Good practice points▸ As gas exchange will improve with increased

alveolar ventilation, NIV settings should be opti-mised before increasing the FiO2.

▸ The flow rate of supplemental oxygen may need tobe increased when ventilatory pressure is increasedto maintain the same SaO2 target.

▸ Mask leak and delayed triggering may be causedby oxygen flow rates >4 L/min, which risks pro-moting or exacerbating patient-ventilator asyn-chrony. The requirement for high flow ratesshould prompt a careful check for patient-ventilator asynchrony.

▸ A ventilator with an integral oxygen blender isrecommended if oxygen at 4 L/min fails tomaintain SaO2 >88%.

Humidification with NIVRecommendation6. Humidification is not routinely required(Grade D).Good practice pointHeated humidification should be considered if thepatient reports mucosal dryness or if respiratorysecretions are thick and tenacious.

Bronchodilator therapy with NIVGood practice points▸ Nebulised drugs should normally be adminis-

tered during breaks from NIV.▸ If the patient is dependent on NIV, bronchodila-

tor drugs can be given via a nebuliser insertedinto the ventilator tubing.

Davidson AC, et al. Thorax 2016;71:ii1–ii35. doi:10.1136/thoraxjnl-2015-208209 ii1

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Sedation with NIVRecommendations7. Sedation should only be used with close monitoring(Grade D).8. Infused sedative/anxiolytic drugs should only be used in anHDU or ICU setting (Grade D).9. If intubation is not intended should NIV fail, then sedation/anxiolysis is indicated for symptom control in the distressed oragitated patient (Grade D).Good practice pointIn the agitated/distressed and/or tachypnoeic individual onNIV, intravenous morphine 2.5–5 mg (± benzodiazepine) mayprovide symptom relief and may improve tolerance of NIV.

NIV complicationsGood practice points▸ Minor complications are common but those of a serious

nature are rare. Patients should be frequently assessed toidentify potential complications of NIV.

▸ Care is needed to avoid overtightening of masks.▸ Previous episodes of ventilator-associated pneumothorax

warrant consideration of admission to HDU/ICU and use ofNIV at lower than normal inspiratory pressures.

▸ The development of a pneumothorax usually requires inter-costal drainage and review of whether to continue with NIV.

Sputum retentionRecommendations10. In patients with neuromuscular disease (NMD), mechanicalinsufflation and exsufflation should be used, in addition tostandard physiotherapy techniques, when cough is ineffectiveand there is sputum retention (Grade B).11. Mini-tracheostomy may have a role in aiding secretion clear-ance in cases of weak cough (NMD/chest wall disease (CWD)) orexcessive amounts (COPD, cystic fibrosis (CF)) (Grade D).

Modes of IMVRecommendations12. Spontaneous breathing should be established as soon as pos-sible in all causes of AHRF (Grade C).13. Controlled IMV may need to be continued in some patientsdue to severe airflow obstruction, weak muscles leading to poortriggering or to correct chronic hypercapnia (Grade C).Good practice pointIn obstructive diseases, controlled IMV should be continueduntil airway resistance falls.

Invasive ventilation strategyRecommendations14. During controlled ventilation, dynamic hyperinflation should beminimised by prolonging expiratory time (I:E ratio 1: 3 or greater)and setting a low frequency (10–15 breaths/min) (Grade C).15. Permissive hypercapnia (aiming for pH 7.2–7.25) may berequired to avoid high airway pressures when airflow obstruc-tion is severe (Grade D).16. Carbonic anhydrase inhibitors should not be routinely usedin AHRF (Grade C).

Positive end expiratory pressureRecommendation17. Applied extrinsic positive end expiratory pressure (ePEEP)should not normally exceed 12 cm (Grade C).

Sedation in IMVRecommendation18. Sedation should be titrated to a specific level of alertness(Grade B).

Patient-ventilator asynchronyRecommendations19. Ventilator asynchrony should be considered in all agitatedpatients (including NIV) (Grade C).20. As patients recover from AHRF, ventilator requirementschange and ventilator settings should be reviewed regularly(Grade C).

Use and timing of a tracheostomyRecommendations21. Performing routine tracheostomy within 7 days of initiatingIMV is not recommended (Grade A).22. The need for and timing of a tracheostomy should be indivi-dualised (Grade D).Good practice points▸ In AHRF due to COPD, and in many patients with NMD or

obesity hypoventilation syndrome (OHS), NIV supportedextubation should be employed in preference to inserting atracheostomy.

▸ In AHRF due to NMD, alongside discussion with the patientand carers, the decision to perform tracheostomy should bemultidisciplinary and should involve discussion with a homeventilation unit.

Management of hypercapnic respiratory failurePrevention of AHRF in AECOPDRecommendations23. In AHRF due to AECOPD controlled oxygen therapy shouldbe used to achieve target saturations of 88–92% (Grade A).Good practice pointControlled oxygen therapy should be used to achive a target sat-uration of 88–92% in ALL causes of AHRF.

Role of NIV in AECOPDRecommendations24. For most patients with AECOPD, the initial managementshould be optimal medical therapy and targeting an oxygen sat-uration of 88–92% (Grade A).25. NIV should be started when pH<7.35 and pCO2 >6.5 kPapersist or develop despite optimal medical therapy (Grade A).

Table 1 SIGN grades of recommendations

A At least one meta-analysis, systematic review, or RCT rated as 1++, anddirectly applicable to the target population; orA body of evidence consisting principally of studies rated as 1+, directlyapplicable to the target population and demonstrating overall consistency ofresults

B A body of evidence including studies rated as 2++, directly applicable to thetarget population and demonstrating overall consistency of results; orExtrapolated evidence from studies rated as 1++ or 1+

C A body of evidence including studies rated as 2+, directly applicable to thetarget population and demonstrating overall consistency of results; orExtrapolated evidence from studies rated as 2++

D Evidence level 3 or 4; orExtrapolated evidence from studies rated as 2+

ii2 Davidson AC, et al. Thorax 2016;71:ii1–ii35. doi:10.1136/thoraxjnl-2015-208209

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26. Severe acidosis alone does not preclude a trial of NIV in anappropriate area with ready access to staff who can perform safeendotracheal intubation (Grade B).27. The use of NIV should not delay escalation to IMV whenthis is more appropriate (Grade C).28. The practice of NIV should be regularly audited to maintainstandards (Grade C).

Starting NIV in COPDGood practice points▸ Arterial blood gas (ABG) measurement is needed prior to

and following starting NIV.▸ Chest radiography is recommended but should not delay ini-

tiation of NIV in severe acidosis.▸ Reversible causes for respiratory failure should be sought and

treated appropriately.▸ At the start of treatment, an individualised patient plan

(involving the patient wherever possible) should documentagreed measures to be taken in the event of NIV failure.

Prognostic features relating to use of NIV in COPDRecommendations29. Advanced age alone should not preclude a trial of NIV(Grade A).30. Worsening physiological parameters, particularly pH andrespiratory rate (RR), indicate the need to change the manage-ment strategy. This includes clinical review, change of interface,adjustment of ventilator settings and considering proceeding toendotracheal intubation (Grade A).Good practice pointIf sleep-disordered breathing pre-dates AHRF, or evidence of itcomplicates an episode, the use of a controlled mode of NIVovernight is recommended.

Duration of NIV in COPDRecommendation31. NIV can be discontinued when there has been normalisationof pH and pCO2 and a general improvement in the patient’scondition (Grade B).Good practice points▸ Time on NIV should be maximised in the first 24 h depend-

ing on patient tolerance and/or complications.▸ NIV use during the day can be tapered in the following

2–3 days, depending on pCO2 self-ventilating, before beingdiscontinued overnight.

Optimising NIV delivery and technical considerationsGood practice pointBefore considering NIV to have failed, always check thatcommon technical issues have been addressed and ventilator set-tings are optimal (table 3).

Indications for IMV in AECOPDRecommendations32. IMV should be considered if there is persistent or deterior-ating acidosis despite attempts to optimise delivery of NIV(Grade A).33. Intubation should be performed in respiratory arrest or peri-arrest unless there is rapid recovery from manual ventilation/provision of NIV (Grade D).34. Intubation is indicated in management of AHRF when it isimpossible to fit/use a non-invasive interface, for example,

severe facial deformity, fixed upper airway obstruction, facialburns (Grade D).35. Intubation is indicated where risk/benefit analysis by anexperienced clinician favours a better outcome with IMV thanwith NIV (Grade D).

Outcome following NIV or IMV in AECOPDRecommendations36. Prognostic tools may be helpful to inform discussion regard-ing prognosis and with regard to the appropriateness of IMVbut with the caveat that such tools are poorly predictive forindividual patient use (Grade B).37. Clinicians should be aware that they are likely to underesti-mate survival in AECOPD treated by IMV (Grade B).38. Clinicians should discuss management of possible future epi-sodes of AHRF with patients, following an epsiode requiringventilatory support, because there is a high risk of recurrence(Grade B).

Acute asthmaRecommendations39. NIV should not be used in patients with acute asthmaexacerbations and AHRF (Grade C).40. Acute (or acute on chronic) episodes of hypercapnia maycomplicate chronic asthma. This condition closely resemblesCOPD and should be managed as such (Grade D).

Non-CF bronchiectasisRecommendations41. In patients with non-CF bronchiectasis and AHRF, con-trolled oxygen therapy should be used. (Grade D)42. In patients with non-CF bronchiectasis, NIV should be startedin AHRF using the same criteria as in AECOPD (Grade B).43. In patients with non-CF bronchiectasis, NIV should usuallybe tried before resorting to IMV in those with less severephysiological disturbance (Grade C).44. In non-CF bronchiectasis, the patient’s clinical conditionprior to the episode of AHRF, and the reason for the acutedeterioration, should be evaluated and used to inform thedecision about providing IMV (Grade C).Good practice points▸ In patients with non-CF bronchiectasis, the precipitating

cause is important in determining short-term prognosis.▸ Health status prior to the episode of AHRF is an important

predictor of outcome.

Cystic fibrosisRecommendations45. In patients with CF, controlled oxygen therapy should beused in AHRF (Grade D).46. In patients with CF, NIV is the treatment of choice whenventilatory support is needed (Grade C).47. In patients with CF, specialised physiotherapy is needed toaid sputum clearance (Grade D).48. In patients with CF, a mini-tracheostomy combined withNIV may offer greater chance of survival than resorting to IMV.(Grade D)

Restrictive lung diseasesNMD and CWDRecommendations49. Controlled oxygen therapy should be used in patients withNMD or CWD and AHRF (Grade D).


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50. NIV should almost always be trialled in the acutely unwellpatients with NMD or CWD with hypercapnia. Do not wait foracidosis to develop (Grade D).51. In patients with NMD or CWD, NIV should be consideredin acute illness when vital capacity (VC) is known to be <1 Land RR >20, even if normocapnic (Grade D).52. In patients with NMD or CWD, consider controlled ventila-tion as triggering may be ineffective (Grade D).53. In NMD or CWD, unless escalation to IMV is not desiredby the patient, or is deemed to be inappropriate, intubationshould not be delayed if NIV is failing (Grade D).Good practice points▸ Individuals with NMD and CWD who present with AHRF

should not be denied acute NIV.▸ NIV is the ventilation mode of choice because patients with

NMD or CWD tolerate it well and because extubation fromIMV may be difficult.

▸ In patients with NMD or CWD, deterioration may be rapidor sudden, making HDU/ICU placement for therapy moreappropriate.

▸ In patients with NMD or CWD, senior/experienced input isneeded in care planning and is essential if differences inopinion exist or develop between medical staff and patientrepresentatives.

▸ In patients with NMD, it should be anticipated that bulbardysfunction and communication difficulties, if present, willmake NIV delivery difficult, and may make it impossible.

▸ Discussion about NIV and IMV, and patients’ wishes withrespect to cardiopulmonary resuscitation, should occur aspart of routine care of patients with NMD or CWD.

▸ In patients with NMD or CWD, nocturnal NIV shouldusually be continued following an episode of AHRF, pendingdiscussion with a home ventilation service.

NIV failure and discontinuing NIV following recovery in NMD andCWDGood practice points▸ In patients with NMD or CWD, intolerance of the mask and

severe dyspnoea are less likely to cause NIV failure. Bulbardysfunction makes NIV failure more likely.

▸ Deterioration in patients with NMD or CWD may be verysudden. Difficulty achieving adequate oxygenation or rapiddesaturation during a break from NIV are important warningsigns.

▸ In patients with NMD or CWD, the presence of bulbar dys-function, more profound hypoxaemia or rapid desaturationduring NIV breaks, suggests that placement in HDU/ICU isindicated.

IMV in NMD/CWDRecommendations54. In patients with NMD or CWD, senior staff should beinvolved in decision-making, in conjunction with home mechan-ical ventilation specialists, if experience is limited, and especiallywhen the appropriateness of IMV is questioned (Grade D).55. Advance care planning, particularly around the potentialfuture use of IMV, is recommended in patients with progressiveNMD or CWD. This may best be supported by elective referralto a home ventilation service (Grade D).

IMV strategy in NMD and CWDGood practice points▸ Patients with NMD usually require low levels of PS.▸ Patients with chest wall deformity usually require higher

levels of PS.

▸ PEEP in the range of 5–10 is commonly required to increaseresidual volume and reduce oxygen dependency in bothpatient groups.

Obesity hypoventilation syndromeRecommendations56. Controlled oxygen therapy should be used in patients withOHS and AHRF (Grade D).57. In patients with OHS, NIV should be started in AHRF usingthe same criteria as in AECOPD (Grade B).58. NIV is indicated in some hospitalised obese hypercapnicpatients with daytime somnolence, sleep disordered breathingand/or right heart failure in the absence of acidosis (Grade D).

NIV settings and placement in OHSGood practice points▸ High inspiratory positive airway pressure (IPAP) and expira-

tory positive airway pressure (EPAP) settings are commonlyrequired in patients with OHS (eg, IPAP>30, EPAP>8).

▸ Volume control (or volume assured) modes of providing NIVmay be more effective when high inflation pressures arerequired.

NIV failure in OHSGood practice points▸ Fluid overload commonly contributes to ventilatory failure in

patients with OHS, and its degree is easily underestimated.▸ Forced diuresis may be useful.▸ As the risk of NIV failure is greater, and intubation may be

more difficult, placement in HDU/ICU for NIV isrecommended.

Discontinuing NIV in OHSGood practice points▸ NIV can be discontinued, as in patients with AECOPD.▸ Many patients with AHRF secondary to OHS will require

long-term domiciliary support (CPAP or NIV).▸ Following an episode of AHRF referral to a home ventilation

service is recommended.

IMV strategy in OHSGood practice points▸ In patients with OHS, pressure controlled MV is recom-

mended initially.▸ In patients with OHS, high PEEP settings may be needed to

recruit collapsed lung units and correct hypoxaemia.▸ In patients with OHS, a forced diuresis is often indicated.

Weaning from IMVIntroductionRecommendations59. Treating the precipitant cause of AHRF, normalising pH,correcting chronic hypercapnia and addressing fluid overloadshould all occur before weaning is started (Grade D).60. A brain natriuretic peptide (BNP)-directed fluid manage-ment strategy should be considered in patients with known leftventricular dysfunction. (Grade B)

Weaning methodsRecommendations61. Assessment of the readiness for weaning should be under-taken daily (Grade C).62. A switch from controlled to assisted IMV should be made assoon as patient recovery allows (Grade C).


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63. IMV patients should have a documented weaning plan(Grade B).

Assessing readiness for discontinuation of mechanical ventilationRecommendation64. A 30 min spontaneous breathing trial (SBT) should be usedto assess suitability for extubation (Grade B).65. Factors including upper airway patency, bulbar function,sputum load and cough effectiveness should be considered priorto attempted extubation (Grade D).

Outcome following extubationRecommendation66. Care is needed to identify factors that increase the risk ofextubation failure so that additional support, such as NIV orcough assist, can be provided (Grade B).

Weaning protocolsRecommendations67. Although an organised and systematic approach to weaningis desirable, protocols should be used with caution in patientswith AHRF (Grade B).68. The use of computerised weaning cannot be recommendedin AHRF (Grade D).

Use of NIV in the ICUPlanned NIV to speed weaning from IMVRecommendation69. NIV is recommended to aid weaning from IMV in patientswith AHRF secondary to COPD (Grade B).70. In other causes of AHRF, NIV may have a role in shorteningthe duration of IMV when local expertise in its use exists (and ofcough assist when indicated) and there are features present thatindicate extubation is likely to be successful (Grade D).

NIV in high-risk patientsRecommendation71. Prophylactic use of NIV should be considered to providepost-extubation support in patients with identified risk factorsfor extubation failure (Grade B).

NIV as ‘rescue’ therapy post-extubationRecommendations72. NIV should not be used routinely for unexpected post-extubation respiratory failure (Grade B).73. In COPD, a trial of NIV may be justified for unexpectedpost-extubation respiratory failure where local expertise exists(Grade D).

Care planning and delivery of careAppropriate care environments for the delivery of NIVRecommendations74. NIV services should operate under a single clinical leadhaving formal working links with the ICU (Grade D).75. The severity of AHRF, and evidence of other organdysfunction, should influence the choice of care environment(Grade C).76. NIV should take place in a clinical environment withenhanced nursing and monitoring facilities that are beyondthose of a general medical ward (Grade C).77. Initial care plans should include robust arrangements forescalation, anticipating that around 20% of AHRF cases shouldbe managed in a level 2 or 3 environment (Grade C).

Good practice points▸ A 2–4 bedded designated NIV unit (located within a medical

high dependency area or within a respiratory ward withenhanced staffing levels) provides a sound basis for the provi-sion of NIV in a DGH serving a population of 250 000 andwith an average prevalence of COPD.

▸ Areas providing NIV should have a process for audit andinterdisciplinary communication.

Palliative care and advanced care planningRecommendations78. Clinicians delivering NIV or IMV should have ready accessto palliative medicine (Grade D).79. Multidisciplinary advance care planning should be anintegral part of the routine outpatient management of progres-sive or advanced disease and care plans should be reviewed onpresentation during an episode of AHRF (Grade D).80. The use of NIV may allow time to establish patient prefer-ence with regard to escalation to IMV. (Grade D)

End of life careGood practice points▸ Although removal of the NIV mask may be agreed as prefer-

able, a dignified and comfortable death is possible with it inplace.

▸ Clinicians delivering NIV or IMV should have training inend-of-life care and the support of palliative care teams.

Novel therapiesExtracorporeal CO2 removal (ECCO2R)Recommendations81. If local expertise exists, ECCO2R might be considered:▸ If, despite attempts to optimise IMV using lung protective

strategies, severe hypercapnic acidosis (pH<7.15) persists(Grade D);

▸ When ‘lung protective ventilation’ is needed but hypercapniais contraindicated, for example, in patients with coexistentbrain injury (Grade D);

▸ For IMV patients awaiting a lung transplant (Grade D).Good practice pointECCO2R is an experimental therapy and should only be usedby specialist intensive care teams trained in its use, and whereadditional governance arrangements are in place, or in thesetting of a research trial.

Helium/oxygen ventilationRecommendation82. Heliox should not be used routinely in the management ofAHRF (Grade B).

ABBREVIATIONS AND GLOSSARYABG Arterial blood gasesAECOPD Acute exacerbation of COPDAHRF Acute hypercapnic respiratory failureAPACHE II Acute Physiology and Chronic Health

Evaluation: a severity of illness scoreARDS Acute Respiratory Distress SyndromeBi-level/Bi-PAP Ventilation mode using 2 levels of pressure

supportBMI Body mass indexBODE Body mass index, obstruction, dyspnoea and

exercise tolerance scoreBpm Heart rate (beats per minute)BTS British Thoracic Society


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CF Cystic fibrosisCOPD Chronic obstructive pulmonary diseaseCPAP Continuous positive airways pressureCWD Chest Wall DiseaseDECAF Dyspnoea, Eosinopenia, Consolidation,

Acidaemia and atrial Fibrillation ScoreECCO2R Extra corporeal carbon dioxide removalECG ElectrocardiogramEELV End expiratory lung volumeEPAP Expiratory positive airway pressureePEEP Extrinsic PEEPExpiratorytrigger

Mechanism by which ventilator senses end ofinspiration

FBC Full blood countFFM Full face maskFiO2 Fractional inspired concentration of oxygenFRC Functional residual capacityHDU High Dependency UnitICS Intensive Care SocietyICU Intensive Care UnitIE Ratio Inspiratory/expiratory time ratioIMV Invasive mechanical ventilationIPAP Inspiratory positive airway pressureiPEEP Intrinsic PEEPL/min Litres per minuteNAVA Neurally adjusted ventilatory assistMND Motor neurone diseaseNCROP National Chronic Obstructive Pulmonary

Ddisease Resources and Outcomes ProjectNIV Non-invasive (positive pressure) ventilationNMD Neuromuscular diseaseOHS Obesity hypoventilation syndromeOSA Obstructive sleep apnoeaPAV Proportional assist ventilationpCO2/pO2 Partial pressure of carbon dioxide/oxygenPCV Pressure controlled ventilationPEEP Positive end expiratory pressureePEEP Extrinsic PEEPiPEEP Intrinsic PEEPpH Acid base balanceQoL Quality of lifeRCT Randomised controlled trialRR Respiratory rateSBT Spontaneous breathing trialSaO2 Oxygen saturationTcpCO2 Transcutaneous measurement of pCO2Te Expiratory duration (seconds)Ti Inspiratory duration (seconds)U&E Blood urea and electrolyte valuesVAP Ventilator associated pneumoniaVC Vital capacityVt Tidal volume

INTRODUCTIONBackgroundThe British Thoracic Society (BTS) published the guideline,‘The use of non-invasive ventilation in acute respiratory failure’,in 2002.1 This was in response to trials demonstrating that NIVwas an alternative to IMV in life-threatening respiratory acidosisdue to AECOPD. The guideline drew attention to evidence that,when NIV was used in the less severely unwell patient, it alsolimited progression to more severe respiratory failure.2 The trial

also demonstrated the feasibility, with adequate staff training, ofdelivering NIV on a general medical or admission ward withenhanced support.

In subsequent years, NIV has been shown to deliver betterrather than equivalent outcomes to invasive ventilation inAECOPD (see Management of hypercapnic respiratory failuresection). Although the 2002 guideline recognised NIV to beeffective in other causes of AHRF, the evidence was, basedlargely on an extrapolation from its domiciliary use in neuro-muscular and CWD. In the intervening years, better evidencehas accumulated for the use of NIV in non-COPD disease.Repeated national audits have, however, raised concerns thatexpected patient benefit is not being delivered, and havepointed to a number of process deficiencies.3–5 There is also therisk, in the absence of justifying trial evidence, that the preferreduse of NIV in AECOPD might be extended to all hypercapnicpatients, irrespective of circumstance or underlying diseaseprocess. That this is a real risk might be inferred from the BTSaudits where the indication for NIV was not COPD in over30% of cases.3 4

NIV development in the UK has been largely outside theorganisational ‘umbrella’ of critical care. This may haveadversely affected resource allocation and contributed to a lackof integration in NIV and IMV patient pathways. Other unin-tended consequences might be a restriction on access to invasiveventilation and delay in the development of extended applica-tions of NIV, such as accelerating extubation and its use in themanagement of post-extubation respiratory failure, in ICUs.6

The ‘closed unit’ approach advocated in critical care may alsohave made care of the invasively ventilated respiratory patientthe preserve of the intensivist. Such specialists may have littleexperience of the ability of domiciliary NIV to reverse chroniccardiorespiratory failure and this may lead to underestimatingsurvival, particularly in advanced NMD or CWD.

For these varied reasons, the need for up-to-date guidancewas acknowledged by BTS and the Intensive Care Society (ICS).The aim of the guideline is to draw attention to the evidence ofsuboptimal care in AHRF in the UK, provide an overview of theevidence supporting the use of invasive and non-invasive venti-lation, encourage better communication between admitting clin-icians and critical care services, promote the use of AHRFpatient pathways, and improve resourcing, training, outcomesand patient experience for all adults who develop AHRF.

Definition of AHRFAHRF results from an inability of the respiratory pump, inconcert with the lungs, to provide sufficient alveolar ventilationto maintain a normal arterial PCO2. Co-existent hypoxaemia isusually mild and easily corrected. Conventionally, a pH <7.35and a PCO2 >6.5 kPa define acute respiratory acidosis and,when persisting after initial medical therapy, have been used asthreshold values for considering the use of non-invasive ventila-tion. More severe degrees of acidosis, such as pH<7.25, havebeen used as a threshold for considering provision of IMV.

Importance of AHRFAHRF complicates around 20% of acute exacerbations ofCOPD.2 7 It signals advanced disease, a high risk of future hos-pitalisations and limited long-term prognosis. The median sur-vival following recovery from AHRF was 1 year in a large caseseries.7 Around 12% of patients with hypercapnic COPD diedduring the index admission and this increased to 33% if therespiratory acidosis developed after hospitalisation. In asthma,acute hypercapnia also signals an increased risk of death and an


BTS guidelines




increased likelihood of future life-threatening attacks.8 Thesame risks apply to AHRF complicating CF and bronchiectasis,although this has not been formally reported. In the neuromus-cular and CWDs, including morbid obesity, respiratory pumpfailure is often insidious in its onset, but AHRF may be acuteand unexpected. Acute on chronic ‘decompensated’ episodes ofAHRF are more common and normally indicate the future needfor domiciliary NIV.

Intended use and target audience of the guidelineA central theme of the guideline is to promote integration in theplanning and delivery of NIV and IMV in AHRF. Despite evi-dence demonstrating the value of non-invasive ventilation in themanagement of AHRF, its introduction into routine clinicalpractice in the UK has not delivered the expected patient benefitand it is likely that NIV provision has, inadvertently, reducedaccess to IMV in AECOPD and the other causes of AHRF. Theintroduction, in hospitals accepting acute admissions, of anadequately resourced and integrated AHRF patient pathway isstrongly recommended in the expectation that this will lead toimproved clinical outcomes and patient experiences.

The target audience for the guideline is medical, nursing andphysiotherapy staff working in emergency receiving rooms,medical assessment units, admission wards, respiratory wardsand in high dependency and critical care units. The guidelineapplies to adults. For information on NIV in children withneuromuscular weakness, see the BTS guideline RespiratoryManagement of Children with Neuromuscular Weakness.9

Areas not covered by the guidelineThe guideline does not cover the management of AHRF due tocardiac failure, trauma or acute brain injury. The guideline refersto domiciliary NIV but does not aim to provide guidance onthis. The use of non-invasive ventilation is more extensivelycovered than IMV because the evidence and the clinical experi-ence in its use is recent and because the technical aspects con-cerning IMVare well covered by standard texts.

UnitsIntrathoracic pressure and pressures relating to mechanicalventilation are presented as cm H2O. ABG tensions arepresented as kPa.

Guideline group membersA list of Guideline Group members and BTS Standards of CareCommittee members who assisted with the production of theguideline is given in appendix 1.The Guideline Group members adhered to the BTS and ICSpolicies for the Declaration of Interests and, where appropriate,specific relevant interests are declared in appendix 1.

Methods and terminologyThe guideline has been produced according to the BTSGuideline Production manual and adheres to the criteria set outin the AGREE II instrument.10 11

Clinical questions and literature searchClinical questions were gathered in the PICOT (Patient,Intervention, Comparison, Outcome and Time) format to definethe scope of the guideline and inform the literature search.Systematic electronic database searches were conducted in orderto identify potentially relevant studies for inclusion in the guide-line. For each clinical question, the following databases weresearched: Ovid MEDLINE (including MEDLINE In-Process),

Ovid EMBASE, EMSCO CINAHL, Ovid PsycINFO and theCochrane Library (including the Cochrane Database ofSystematic Reviews, the Database of Abstracts of Reviews ofEffects and the Cochrane Central Register of Controlled Trials).

An initial search was carried out in November 2010, using acombination of indexed and free text terms defining the clinicalquestions that had been agreed as important in formulatingguidelines in AHRF. It was limited to studies after 1990, onadults, in journals published in English and where at least anabstract was available. The searches identified a total of 582potential papers, which were subsequently supplemented bypublications known to members or resulting from additionalsearches undertaken by the writing groups after 2010. The lit-erature search was run again in September 2013, for relevantpublications between 2010 and 2013, yielding a further 308potentially relevant references. Additional references were sub-sequently included from personal collections.

Appraisal of the literatureAppraisal was performed using the criteria stipulated by theAGREE collaboration. Each paper was appraised by at least tworeviewers. The writing lead for each section read the title andabstract of papers identified and agreed with at least onemember of each writing group on whether such a paper wasdefinitely relevant, possibly relevant or not relevant, to thesection. The criteria used were that the paper addressed a clin-ical question, the study method used was satisfactory and thatthe paper was available in English.

Full papers were obtained for all relevant or possibly relevantabstracts. Two members for each section independently appraisedeach paper, using the SIGN critical appraisal checklists. An evi-dence level was assigned to each study using SIGN methodology(table 2). These evidence levels are shown in the evidence tablespresented in the online supplementary appendix 3.

Considered judgement and grading of recommendationsThe guideline group used the evidence tables to judge the bodyof evidence and to develop recommendations for this guideline.Where evidence was lacking, expert opinions were obtained byconsensus. The following were considered in the grading of therecommendations: the number of studies and number ofpatients providing evidence, the applicability of such evidence,and whether generalisable to the patient groups in the guidelineand to UK practice and the degree of strength as judged by theconsistency of evidence obtained to support recommendations.

Table 2 SIGN levels of evidence

1++ High-quality meta-analyses, systematic reviews of RCTs, or RCTs with avery low risk of bias

1+ Well-conducted meta-analyses, systematic reviews or RCTs with a lowrisk of bias

1− Meta-analyses, systematic reviews or RCTs with a high risk of bias2++ High-quality systematic reviews of case control or cohort or studies

High-quality case–control or cohort studies with a very low risk ofconfounding or bias and a high probability that the relationship is causal

2+ Well-conducted case–control or cohort studies with a low risk ofconfounding or bias and a moderate probability that the relationship iscausal

2− Case–control or cohort studies with a high risk of confounding or biasand a significant risk that the relationship is not causal

3 Non-analytic studies, eg, case reports, case series4 Expert opinion

RCT, randomised controlled trial.


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Recommendations were graded from A to D, using the SIGNGrading System (table 2), as indicated by the strength of the evi-dence as listed in the tables. Important practical points that lackresearch evidence were highlighted as ‘Good Practice Points’.Good practice pointsRecommended best practice based on the clinical experience ofthe guideline development group.

Drafting the guidelineThe Guideline Group corresponded regularly. The initialmeeting took place in October 2009, and subsequent meetingsof the full committee occurred in June and November 2010,September 2011, and March and September 2012. Draft docu-ments were reviewed by the BTS Standards of Care Committeeat meetings in 2013 and 2014, and a final draft was producedwith the help and collaboration of members of the BTSStandards of Care Committee in September 2014 to March2015. The guideline was made available for public consultationon the BTS website from 7 May to 12 June 2015. The reviseddocument was reviewed by the BTS Standards of CareCommittee in September 2015 and final approval for publica-tion was given in November 2015.

PRINCIPLES OF MECHANICAL VENTILATIONModes of mechanical ventilationThere are two basic modes of providing mechanical ventilation.In volume-targeted, the operator sets the tidal volume to bedelivered and the duration of inspiration (Ti). The ventilatorgenerates whatever pressure is necessary to deliver this volumewithin this time. In pressure-targeted, the operator sets theinspiratory pressure. The volume of air the patient receives is afunction of the impedance to inflation of the lungs and chestwall and the inspiratory time. The Ti should be of sufficientlength to achieve an adequate volume and at a frequency thatallows the patient time to fully exhale.

The terminology used for pressure-targeted ventilation cancause confusion. In bi-level ventilation, one pressure is set forinspiration (IPAP) and a second pressure for expiration (EPAP).The difference between the two is the level of ventilatory assist-ance or PS. This mode is most commonly used for NIV. Thesame term, CPAP with Pressure Support’, can be used todescribe a mode of invasive ventilation and/or non-invasive ven-tilation on some ICU ventilators. The operator sets an incremen-tal inspiratory pressure above the CPAP setting rather thansetting an absolute level of inspiratory pressure.

Pressure-targeted ventilation has a number of advantages.First, the pressure delivered is constant and this avoids thesudden and uncomfortable pressure increase that occurs withvolume control. Second, pressure-targeted ventilation compen-sates for air leak,12 13 which is an inevitable consequence of theinterfaces used for NIV. Third, positive pressure throughoutexpiration (EPAP) flushes exhaled CO2 from the mask and distalventilator tubing,14 15 aids triggering (see below) and counter-acts the tendency for upper airway collapse during expiration.Pressure ventilators have been used in almost all of the rando-mised controlled trials (RCTs) in AHRF.16 In the UK, volumeventilators are rarely employed (outside of specialist centres)and will not be considered further in this guideline.

In the Spontaneous (S) mode (also known as assist mode), theventilator delivers assisted breaths in response to patient inspira-tory effort. If the patient fails to make adequate inspiratory effort,no ventilator support is delivered. By contrast, in the timed (T)mode (also known as control mode), the ventilator deliversbreaths at a rate set by the operator regardless of patient

inspiratory effort. ‘Pressure-controlled ventilation’ (PCV) is theterm used to describe a mode in which the operator sets theinspiratory pressure, the length of inspiration and the inspiratoryrate. In the spontaneous/timed (S/T) mode (also known as assistcontrol), a backup rate is set by the operator. If the patient’s RR isslower than the backup rate, machine-determined breaths will bedelivered (ie, controlled ventilation). If the patient breathes fasterthan the backup rate, no machine determined breaths will bedelivered and all breaths will be triggered (or assisted). The pro-portion of controlled and assisted breaths often varies, dependingon the patient’s state of alertness and respiratory drive.

Trigger sensitivity refers to the effort required by the patientto initiate, or trigger, the ventilator. The lower the trigger sensi-tivity, the greater effort the patient needs to make to trigger asupported breath. Different trigger settings may be required forindividual causes of AHRF (see Management of hypercapnicrespiratory failure section).

S/T is the NIV mode most commonly employed in treatingAHRF. There have been no trials comparing PS ventilation andPCV in the treatment of AHRF. Bench studies suggest that venti-lators designed specifically for NIV have superior performanceover standard ICU ventilators used to deliver NIV, particularlyin the presence of significant leak.17–22 The extent to whichindividual types of ICU ventilators (set in the NIV mode) cancompensate for leak and the adequacy of patient triggeringvaries.23 Generally, ICU ventilators appear more prone topatient-ventilator asynchrony than home care ventilators.24

Evidence statementMost RCTs that demonstrate an advantage to NIV in AHRFhave used pressure targeted ventilators (Level 1+).Recommendation1. Pressure targeted ventilators are the devices of choice foracute NIV (Grade B).Good practice points▸ Both PS and pressure control modes are effective.▸ Only ventilators designed specifically to deliver NIV should

be used.

Choice of interface for NIVThe FFM is the most suitable interface, as mouth breathing pre-dominates in AHRF. To accommodate the natural diversity ofthe human face, a range of shapes and sizes of FFM should beavailable. Reported studies suggest that different types of inter-faces do not affect outcome, but the trials have been small andcomparison of masks has been inadequately powered to detect adifference.25–37 The helmet interface, which covers the wholehead, is an alternative to an FFM,38–44 but triggering is ineffect-ive. Patients may report about noise caused by turbulence withinthe helmet,45 and it is not possible to provide humidified gasesbecause of ‘rain out’ in the helmet. A mask that covers thewhole of the face (including the eyes, but not the ears) is usefulwhen air leak remains excessive or when nasal bridge ulcerationdevelops,46 and is sometimes better tolerated by the confused oragitated patient. In those who find the FFM claustrophobic ordistressing, experienced practitioners may consider using a nasalmask or nasal pillows. Mouth leak limits the effectiveness ofnasal interfaces during sleep and nasal pillows are more easilydislodged than the FFM.

Ventilators designed for NIV usually employ a single lumencircuit whereas IMV ventilators use a dual lumen circuit (separ-ate tubing for inhalation and exhalation). In the former, a maskwith an integral exhalation port is commonly used. If not, anexhalation port needs to be inserted into the ventilator circuitclose to the mask. A minimum EPAP of 3 cm is required to vent


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exhaled air.14 47 The website http://ersbuyersguide.org/ offersinformation on NIV interfaces that are currently available.Evidence statementAn FFM is the interface of choice for general/non-specialist use(Level 4).Recommendation2. An FFM should usually be the first type of interface used(Grade D).Good practice points▸ A range of masks and sizes is required, and staff involved in

delivering NIV need training in and experience of usingthem.

▸ NIV circuits must allow adequate clearance of exhaled airthrough an exhalation valve or an integral exhalation port onthe mask.

Indications for and contra-indications to NIV in AHRFThe indication for NIV will vary according to the underlyingcause, severity of illness and associated complicating factors.Broad criteria can be used and are summarised in figure 1, andfurther discussed in Management of hypercapnic respiratoryfailure section. Severe facial deformity, fixed upper airwayobstruction or facial burns, will occasionally make NIV impos-sible. A number of other contra-indications have been suggested(see figure 1).48 These have most often been employed as exclu-sion criteria in clinical trials rather than being definitively shownto result in a worse outcome.16 Some of the criteria have beenchallenged. For instance, coma has been regarded as an absolutecontra-indication, because of its associated loss of airway protec-tion, but Diaz et al49 report similar outcomes with NIV in thosewith a Glasgow Coma Score <8 as the outcomes found in morealert patients. Similarly, confusion, agitation and cognitive

impairment make NIV more difficult to apply but should notpreclude its use.

There is less haemodynamic compromise with NIV than withIMV, and hypotension should rarely preclude using NIV.Significant arrhythmia, especially if causing hypotension, maytip the balance towards preferring intubation as, in these cir-cumstances, cardioversion may be indicated.

An acute pneumothorax should be drained before applyingNIV. If it is too small to allow the safe placement of a chestdrain (or is suspected to be chronic) NIV may proceed withcareful monitoring. Using a lower inflation pressure seems theor-etically sensible but is without evidence. If the patient deterio-rates, NIV should be discontinued—in case it is contributing tothe development of a tension pneumothorax—and an urgentchest radiograph obtained.

Vomiting has been considered a contra-indication. The keyissue is whether the NIV mask can be rapidly removed, that is,an assessment of whether the patient can signal the need tovomit. Marked abdominal distension may sometimes precipitateAHRF in individuals at risk, for example in COPD or morbidobesity. Management should then address the underlying causeof abdominal distension and manage the risk of vomiting byinserting a nasogastric tube. Similarly, in the at-risk patient,hypercapnic respiratory failure may complicate the later stagesof pregnancy (eg, kyphoscoliosis or muscular dystrophy). NIV isideally suited to manage this complication. The need for NIVshould be electively assessed (by nocturnal monitoring), butmask ventilation can be initiated during delivery should respira-tory distress develop in an at-risk patient.The presence of copious secretions increases the risk of treat-ment failure,50 but NIV may also improve the ability to clearsecretions and improve alveolar ventilation.51 52

Figure 1 Summary for providing acute non-invasive ventilation.


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http://ersbuyersguide.org/

http://ersbuyersguide.org/



Respiratory arrest or peri-arrest have been considered as abso-lute contra-indications as NIV is intended to supplement spon-taneous breathing. However, as bag and mask ventilation (itselfa form of NIV) is used as a prelude to intubation, a short trialof NIV by an experienced operator, can be justified whilepaying special attention to the risk of glottic occlusion.In summary, the presence of adverse features is an indication formore intense monitoring and placement within HDU/ICUrather than a contra-indication per se.Evidence statementThere are few absolute contra-indications to a trial of NIV butsome adverse features, especially when combined, require morecaution and more intense monitoring (Level 4).The presence of adverse features increases the risk of NIVfailure (Level 2++).Recommendation3. The presence of adverse features increases the risk of NIVfailure and should prompt consideration of placement in HDU/ICU (Grade C).Good practice points▸ Adverse features should not, on their own, lead to withhold-

ing a trial of NIV.▸ The presence of relative contra-indications necessitates a

higher level of supervision, consideration of placement inHDU/ICU and an early appraisal of whether to continueNIVor to convert to IMV.

Monitoring during NIVContinuous monitoring of oxygen saturation is essential.Repeated measurement of ABG tensions will be required andcan be assessed by capillary sampling or intermittent arterialpuncture, noting that capillary sampling is less painful for thepatient.53 54 One advantage of HDU/ICU placement may be toallow the safe use of an indwelling arterial line for blood sam-pling. Transcutaneous pCO2 (TcpCO2) monitoring is a com-monly employed investigation in home ventilation units and thedevices are increasingly being employed in hospitals.Small studies have reported on its use in acute respiratoryacidosis.55–57 A study by van Oppen et al58 reported on10 patients receiving acute NIV and demonstrated that TcpCO2

monitoring is reliable over 12 h and provides an adequateestimation of pH. Further studies are needed to assess the roleof transcutaneous CO2 monitoring.

ECG monitoring is advised for all patients with a tachycardia>120 bpm, dysrhythmia or known cardiomyopathy. As in allseverely ill patients, serial vital signs (and National EarlyWarning Scores, where implemented) should be recorded.Good practice points▸ Oxygen saturation should be continuously monitored.▸ Intermittent measurement of pCO2 and pH is required.▸ ECG monitoring is advised if the patient has a pulse rate

>120 bpm or if there is dysrhythmia or possiblecardiomyopathy.

Supplemental oxygen therapy with NIVThere are no trials to guide the use of oxygen enrichment. It iswell recognised that hyperoxygenation is harmful in the self-ventilating patient with AHRF.59–61 In the absence of harmfrom modest hypoxaemia, and to avoid confusion that mightarise from having different target saturations in different condi-tions, a saturation range of 88–92% is recommended in allpatients with AHRF either spontaneously breathing or when

receiving NIV.62 This is usually easily achieved in AECOPD, butsevere hypoxaemia may complicate AHRF in other causativediseases such as CWD.

As for the best method of supplying oxygen, Padkin andKinnear,63 in a study of patients who were not acutely unwell,reported no difference in inspired content whether delivereddirectly into the NIV mask or into the ventilator tubing close tothe mask. Introducing oxygen at the ventilator end of the tubingwas less effective. The mean FiO2 achieved was 31% at 1 L/min,37% at 2 L/min, 40% at 3 L/min and 44% at 4 L/min. Flowrates >4 L/min provided minimal additional increase. Kaul64

found that the higher the inspiratory pressure, the less add-itional benefit resulted from higher flow rates (because higherpressures increase leak). High flow rates also resulted in delaytriggering the ventilator. As this risks promoting patient ventila-tor asynchrony, technically advanced NIV ventilators that allowprecise oxygen blending (and a higher FiO2 enrichment) are asafer and more appropriate alternative when hypoxaemia issevere.Evidence statementsIn AHRF-targeted oxygen therapy (SaO2 88–92%) reduces mor-tality (Level 1+).When providing NIV, oxygen enrichment is best given at ornear the mask (Level 3).Recommendations4. Oxygen enrichment should adjusted to achieve SaO2 88–92% in all causes of AHRF being treated by NIV (Grade A).5. Oxygen should be entrained as close to the patient as possible(Grade C).Good practice points▸ As gas exchange will improve with increased alveolar ventila-

tion, NIV settings should be optimised before increasing theFiO2.

▸ The flow rate of supplemental oxygen may need to beincreased when ventilatory pressure is increased to maintainthe same SaO2 target.

▸ Mask leak and delayed triggering may be caused by oxygenflow rates >4 L/min, which risks promoting or exacerbatingpatient–ventilator asynchrony. The requirement for high flowrates should prompt a careful check for patient–ventilatorasynchrony.

▸ A ventilator with an integral oxygen blender is recommendedif oxygen at 4 L/min fails to maintain SpO2 >88%.

Humidification with NIVThere is no evidence to guide the use of humidification in acuteNIV. Heated humidification may reduce upper airway resistanceand increase comfort when leak is high.65 In short-term studies,heated humidification reduces upper airway dryness,66 67 whichmight improve tolerance and aid secretion clearance, but thishas not been proven. Humidification should only be consideredwhen upper airway dryness is a problem or secretions are diffi-cult to expectorate.Evidence statementNo evidence exists to guide humidification practice in acuteNIV (Level 4).Recommendation6. Humidification is not routinely required (Grade D).Good practice pointHeated humidification should be considered if the patientreports mucosal dryness or if respiratory secretions are thickand tenacious.


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Bronchodilator therapy with NIVAs part of a PhD thesis, Kaul68 found that nebulised bronchodi-lators given concomitantly with NIV in stable patients producedless benefit than when given while patients were breathing spon-taneously. Brief discontinuation of NIV for the administrationof bronchodilators appears to be safe.69 Acccordingly, broncho-dilator therapy is probably better given during breaks in NIV.This may also facilitate coughing and the clearing of respiratorysecretions. If discontinuing NIV results in patient distress, itshould be continued and a nebuliser sited proximally in thecircuit.70

Good practice points▸ Nebulised drugs should normally be administered during

breaks from NIV.▸ If the patient is dependent on NIV, bronchodilator drugs can

be given via a nebuliser inserted into the ventilator tubing.

Sedation with NIVPatient agitation and distress are common in AHRF and may bemade worse by the application of NIV before gas exchange hasimproved and the patient has sensed a reduction in the work ofbreathing. Despite this, sedatives/anxiolytics and/or opiates areinfrequently used due to concern about depressing respiratorydrive. This is understandable if NIV is delivered in an inappro-priate environment that is unable to provide continuous moni-toring and that does not have the ready availability of medicalstaff to perform safe intubation if needed. On the contrary,relieving patient distress is an important goal and might beexpected to increase comfort and the success of NIV. In a 2007survey of members of the critical care assemblies of theAmerican College of Chest Physicians and the EuropeanRespiratory Society, respondents reported using sedatives oropiates in only 25% of cases and 21% stated they had neverused either.71 The risk of respiratory depression was given asthe reason for non-use. Individual practice was highly variableand, as the response rate was poor (42% European, 14% NorthAmerican), the conclusions reported are more qualitative thanquantative. When treatment was given it was mostly by bolusinjection and rarely according to a sedation protocol. Greaterexperience in the use of NIV and being a critical care clinicianincreased reported use of opiates/sedation.

In the 2013 BTS audit, involving 2693 cases, NIV failed toreverse AHRF in 30% of patients.5 Agitation was reported asthe principal reason in 31% of these. Sedation was ‘attempted’in 84%. No details are available on what agents were used, oroutcome in those so treated. As 91% of all NIV treatments wereprovided outside of the HDU/ICU, it appears sedation is nowmore commonly employed but in a potentially unsafeenvironment.

In the ICU setting, case series have reported that infusions ofpropofol,72 dexmedetomidine73 and remifentanyl74 75 are safe,improve comfort and reduce the failure rate of NIV. Senogluet al76 compared infusions of dexmedetomidine and midazolamin 45 AECOPD cases with AHRF, using a protocol aiming at astandard degree of sedation. No differences were found ineffectiveness between the two agents. There were no significantadverse events and no patient failed to improve with NIV. Inanother report, the addition of infused dexmedetomidine to astandard protocol of ‘as needed’ bolus intravenous midazolamand fentanyl, given according to a sedation protocol, failed toshow benefit, but sedation goals were readily achieved and therewas good NIV tolerance and success with the standard proto-col.77 A review of sedation to facilitate NIV tolerance makes the

pharmacological case for preferring an opiate to a benzodiazep-ine (because the latter promotes upper airway obstructionthrough inhibiting the pharangeal dilating muscles) but con-cluded that studies to date have been too small, have used differ-ent drugs and therapy regimes and employed a variety ofoutcome measures.78 Guidance on the use of sedation withinhospitals might be expected to improve patient safety whenimplemented.79

Evidence statementsPatient distress is common in AHRF and often made initiallyworse by applying NIV (Level 4).There is inadequate evidence to guide the use of sedation/anxio-lysis in acute NIV. Their use in a critical care setting is reportedto improve outcome and reduce patient distress (Level 2−).Recommendations7. Sedation should only be used with close monitoring(Grade D).8. Infused sedative/anxiolytic drugs should only be used in anHDU or ICU setting (Grade D).9. If intubation is not intended should NIV fail, then sedation/anxiolysis is indicated for symptom control in the distressed oragitated patient (Grade D).Good practice pointIn the agitated/distressed and/or tachypnoeic individual on NIV,intravenous morphine 2.5–5 mg (± benzodiazepine) mayprovide symptom relief and may improve tolerance of NIV.

NIV complicationsThe reported rate of complications varies widely. One reviewgives an incidence between 30% and 50%,80 the range partlydepending on how a complication is defined. Extended durationof NIV, patient agitation and the frequent need to adjust maskfit are all associated with an increase in rate/severity ofmask-related problems.

Nasal bridge ulceration is the most common problem (5–10%)and may be severe enough to result in NIV failure.81 Over-tightening is a common cause. NIV masks are designed to mouldto the face when pressurised which over-tightening impairs.Should signs of skin trauma become apparent, a barrier dressingand a strategy of regular breaks and alternating between twointerface types should be used. Latex allergy occasionally resultsin florid skin reactions. Some patients seem especially prone tomask-related rash even in the absence of allergy. Topical steroidsmay be indicated and/or antibiotics if the wound becomesinfected.

NIV may cause severe gastric distension. It usually indicatespoor coordination between patient and ventilator and it may benecessary to insert a nasogastric tube. Sinus or ear discomfortand nasal mucosal congestion or drying/ulceration can all occur.The value of humidification in preventing these side effects isuncertain but water-based nasal gels and topical corticosteroidsor decongestants can be used. Petroleum-based emollientsshould not be used with supplemental oxygen.

An acute pneumothorax may be life-threatening but difficultto detect. The development of unexplained agitation/distressor chest pain requires this complication to be excluded.82

Co-existent interstitial lung disease or previous episodes ofspontaneous or ventilator-induced pneumothorax increase therisk. Using a lower IPAP to avoid large tidal volumes, and alower EPAP to avoid significantly increasing end-expiratorylung volume (EELV), are logical but not evidence based. If apneumothorax develops, intercostal drainage is usuallyrequired.


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Good practice points▸ Minor complications are common but those of a serious

nature are rare. Patients should be frequently assessed toidentify potential complications of NIV.

▸ Care is needed to avoid overtightening of masks.▸ Previous episodes of ventilator-associated pneumothorax

warrant consideration of admission to HDU/ICU and use ofNIV at lower than normal inspiratory pressures.

▸ The development of a pneumothorax usually requires inter-costal drainage and review of whether to continue with NIV.

Sputum retentionSputum retention can be a precipitant for AHRF, can cause NIVto fail and is a common reason for respiratory distress post-extubation in patients initially managed by IMV. Excessivesputum production characterises bronchiectasis and CF, andcomplicates some patients with AECOPD. Promoting sputumclearance can be particularly challenging in those with NMDand in the morbidly obese. Techniques, such as manuallyassisted cough and mechanical insufflation–exsufflation (MI-E),aid sputum clearance in patients with NMD.83 84 However, in astudy including patients with either scoliosis or COPD, MI-Ereportedly had no benefit.85 In another RCT, the use of MI-Ereduced post-extubation respiratory failure in a mixed group ofpatients including some with AHRF.86 This study also providedNIV to those in respiratory distress. The reader is referredto the BTS Physiotherapy Guidelines87 for more detailedinformation.

Mini-tracheostomy facilitates secretion clearance in the spon-taneously breathing patient88 and may have a role when sputumretention is thought to be a major determinant of AHRF, suchas in CF. It is not an easy technique to perform in the anxiousand breathless patient and training opportunites are rare.Clinicians who insert percutaneous tracheostomies are bestplaced to provide a service and the HDU/ICU is the best envir-onment in which to perform mini-tracheostomy. In an attemptto avoid intubation, a combination of respiratory support byNIV and suctioning via a mini-tracheostomy has been described.This probably only has application if IMV is not desired by thepatient as, in most such cases, IMV offers more chance of a suc-cessful outcome. In the patient initially managed by IMV, amini-tracheostomy may be inserted at the time of endotrachealtube decannulation in patients with a high secretion load and/ora poor cough.Evidence statementsManual-assisted cough and MI-E are safe methods for aidingsecretion clearance (Level 1+).MI-E is more effective than manual-assisted cough in patientswith stable NMD (Level 2+).Mini-tracheostomy is a useful bedside procedure that can mark-edly improve secretion clearance, but requires patient cooperationand a skilled operator to be performed safely (Level 4).Recommendations10. In patients with NMD, mechanical insufflation and exsuffla-tion should be used, in addition to standard physiotherapy tech-niques, when cough is ineffective and there is sputum retention(Grade B).11. Mini-tracheostomy may have a role in aiding secretion clear-ance in cases of weak cough (NMD/CWD) or excessive amounts(COPD, CF), (Grade D).

Modes of IMVCritical care ventilators are complex devices capable of deliver-ing multiple modes.89 90 The traditional divide between

pressure and volume has become blurred and hybrid modescombine aspects of both. Most patients with AHRF do notrequire sophisticated modes of providing IMV.

Initially, when airway resistance is high and/or compliance islow (eg, in asthma, CF or bronchiectasis) a period of mandated or‘controlled mechanical ventilation’, often combined with deepsedation to reduce spontaneous breathing effort, allows time forbronchodilators, steroids and antibiotics to treat airway inflamma-tion, overcome infection and for ‘bronchial toilet’ to be provided.These considerations also variably apply to the restrictive causes ofAHRF. In addition, poor triggering, because of muscular weak-ness, is a risk in patients with NMD in whom a prolonged periodof controlled mechinical ventilation may be necessary. In allpatients with AHRF, allowing restorative sleep is important.91–93

Management should shift towards supporting rather thanmandating the pattern of ventilation as recovery begins. If thereis adequate spontaneous effort, and the RR is not excessive, aswitch to PS is recommended to reduce the need for sedationand also as the risk of respiratory muscle wasting may bereduced by establishing early spontaneous breathing. Theconcept that suppressing spontaneous breathing is causallyrelated to diaphragm wasting is contentious in the literature.Space constraints prevent a fuller examination. One initiallycompelling human study that claimed to have demonstrated‘disuse atrophy’ was subsequently critised because the dia-phragms had been denervated.94 A study in patients with adultrespiratory distress syndrome (ARDS) reported that thosepatients allowed to breathe spontaneously had less need for sed-ation than patients treated with controlled IMV, a reducedrequirement for vasopressors, fewer days of ventilatory support,earlier extubation and a shorter length of ICU stay.95 This strat-egy has not been assessed in AHRF.Evidence statementsEstablishing early spontaneous breathing reduces the need forsedation, improves cardiac function and reduces the duration ofIMV in ARDS (Level 1−).Recommendations12. Spontaneous breathing should be established as soon as pos-sible in all causes of AHRF (Grade C).13. Controlled IMV may need to be continued in some patientsdue to severe airflow obstruction, weak muscles leading to poortriggering or to correct chronic hypercapnia (Grade C).Good practice pointIn obstructive diseases, controlled IMV should be continueduntil airway resistance falls.

Invasive ventilation strategyIn obstructive causes, tidal volume (Vt) is limited by the airflowobstruction and compounded by the mechanical disadvantage ofhyperinflation. The use of high inflation pressures, to achieve a‘normal’ Vt, risks dynamic hyperinflation.96 It most dramaticallyoccurs soon after intubation but may develop on switching ven-tilation mode, for example, from controlled to assistedventilation.97

The adverse consequences of hyperinflation include baro-trauma, impaired gas exchange and patient discomfort. Theincreased intrathoracic pressure impedes venous return andincreases right ventricular afterload with a resulting fall incardiac output and hypotension.98

Prolonging expiratory time limits gas trapping and is achievedby shortening the inspiratory time and reducing the minutevolume, an approach recommended in airflow obstruction.99 100

If significant gas trapping still occurs, the recommendation is touse a lower than normal Vt in combination with a low RR and


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a more prolonged expiratory phase.99 100 This can often onlybe achieved using a controlled ventilation mode combined withdeeper levels of sedation. On switching to PS (assist) duringrecovery, the inspiratory pressure needs to be sufficient toprovide adequate tidal volume but not excessive. Settings there-fore need to be individually adjusted and require regular review.

In ARDS, over-distention and repetitive recruitment/de-recruitment of lung units causes alveolar damage (so-calledventilator-induced lung injury) and may even provoke systemicinflammation.101 One explanation for improved outcome withlow Vt ventilation (<6 mL/kg), compared with conventionalpractice, may be avoidance of ventilator-induced lung injury.102

The ARDS literature provides evidence for permissive hypercap-nia, demonstrating that a pH above 7.2 is well tolerated.103 Thisis the consensus target when pH control is difficult.89 90

Allowing permissive hypercapnia will result in cerebral vasodila-tion and a rise in intracranial pressure and may also compromisemyocardial contractility. Attempts to raise pH to >7.2 may,however, compound hyperinflation and barotrauma. In ARDS, apeak airway pressure of 30 cm is the usual trigger for employingpermissive hypercapnia, a strategy that reduces mortality.104

In AECOPD, attempts to rapidly restore pO2 and pCO2 tonormal are unnecessary. Although there is little evidence toprovide guidance, it is suggested that the higher the pre-morbidpCO2 (inferred by a high admission bicarbonate), the higher thetarget pCO2 should be. Recovery from extreme levels of hyper-capnia is recognised.105 Any metabolic causes of acidosis, forexample, from insulin insensitivity or excessive B2 stimulatedglycogenolysis, should be treated separately.

In NMD, an adequate tidal volume can be achieved with rela-tively low inflation pressures (eg, 10–15), but higher pressure isneeded in CWD because of reduced chest wall compliance.Lung recruitment strategies (ie, increasing PEEP) should be con-sidered when there is persisting hypoxia and/or evidence of pre-mature small airway closure in dependent lung tissue.Controlled MV may need to be continued in NMD when trig-gering is likely to be inadequate or tiring.

Reducing the bicarbonate buffering capacity will require aperiod of relative hyperventilation when hypercapnia is chronic.The resulting urinary bicarbonate loss resets central respiratorydrive. Carbonic anhydrase inhibitors can be used but caution isneeded as high doses produce unpredictable effects throughcentral stimulation of breathing.106 107

Evidence statementsIn ARDS, a low Vt strategy improves survival (Level 1+).In airflow obstruction, prolonging the expiratory time reducesdynamic hyperinflation (gas-trapping) (Level 2+).

Recommendations for IMV in obstructive disease14. During controlled ventilation, dynamic hyperinflationshould be minimised by prolonging expiratory time (I:E ratio1:3 or greater) and setting a low frequency (10–15 breaths/min)(Grade C).15. Permissive hypercapnia (aiming for pH 7.2–7.25) may berequired to avoid high airway pressures when airflow obstruc-tion is severe (Grade D).16. Carbonic anhydrase inhibitors should not be used routinelyin AHRF. (Grade C).

Positive end expiratory pressurePEEP is an area of physiology that causes confusion amonghealthcare professionals. The best way to set optimal PEEPremains contentious. Simply stated, PEEP shifts the lungs to amore compliant portion of the pressure–volume curve. Inrestrictive causes of AHRF, lung volume is usually reduced andthere may be dependent lung that is poorly ventilated or inwhich there is no effective alveolar ventilation. In these circum-stances, increasing external PEEP increases Vt for a giveninspiratory pressure, will reduce pCO2 and improve oxygen-ation. In obstructive disease, PEEP improves expiratory airflow,limits dynamic hyperinflation and improves alveolar ventila-tion.108 109 Dynamic hyperinflation may be suspected by a pro-gressive fall in tidal volume with constant ventilator pressuresettings (or, with volume control, an increase in inflation pres-sure) and by signs of increasing patient distress such as tachycar-dia and hypotension.

The degree of intrinsic PEEP (iPEEP) can be estimated byexamination of the expiratory flow curve and pressure110 or bemeasured invasively.111 112 Active expiratory muscle contraction,common in airflow obstruction, will artificially increase appar-ent iPEEP. Levels of iPEEP in obstructive airways disease havebeen reported to range from 4.6 to 13.6 cm H2O.113

Setting the PEEP level in excess of iPEEP may be deleterious.This has led to the recommendation that PEEP be set at 50–80% of iPEEP.114 115 However, as the severity of airway obstruc-tion in small airways will vary throughout the lung, a variableresponse to increasing the PEEP might be anticipated. If, onbalance, an increase in ePEEP were to reduce overall airwayresistance then EELV will fall even though ePEEP apparentlyexceeds iPEEP.116 117

Intrinsic PEEP is a pressure that must be overcome by patienteffort before a breath can be triggered. It is, therefore, aninspiratory threshold load and may lead to ineffective triggeringand patient discomfort. Offsetting iPEEP by increasing the ven-tilator PEEP will then reduce the effort of triggering and

Figure 2 Guide to initial settingsand aims with invasive mechanicalventilation.


BTS guidelines




improve patient–ventilator asynchrony.118–120 It is important toappreciate that the same pathophysiological processes occurduring treatment with NIV when a higher EPAP setting mayimprove triggering, patient comfort and oxygenation.Evidence statementIn obstructive causes of AHRF, PEEP may increase tidal volume,improve compliance and reduce airflow obstruction (Level 2+).Setting PEEP greater than iPEEP can be harmful (Level 2+).In restrictive causes of AHRF, PEEP may assist in lung recruit-ment, improve compliance and correct hypoxaemia (Level 3).Recommendation17. Applied ePEEP should not normally exceed 12 cm(Grade C).

Sedation in IMVPatients receiving IMV require sedation, especially before stabil-ity is achieved.89 Most ICUs use Propofol or a benzodiazepine,either alone or in combination with an opioid. Benzodiazepineswith inactive metabolites and/or short acting synthetic opioidshave been recommended to avoid over-sedation.121 122

Although sedation increases IMV tolerance, over-use is asso-ciated with adverse outcomes such as prolonged duration ofIMV, increased ICU length of stay and delirium.123

To avoid this, withholding of further sedation until an object-ive degree of wakefulness develops has been investigated. In twotrials, this strategy was shown to reduce duration of IMV andICU length of stay.124 125 Studies employing sedation protocolstargeting specific (higher) levels of alertness have also reported areduction in duration of IMV, ICU and hospital length ofstay.126–129 However, a meta-analysis of RCTs on sedationbreaks demonstrated safety but failed to confirm benefit,130 anda more contemporary RCT, combining protocolised sedationwith daily breaks, also found no benefit.131 No study has shownharm from sedation breaks. The effect of stopping or reducingsedation on patient experience has not been reported.Evidence statementsDaily interruption of sedation is safe and may reduce the dur-ation of IMVand ICU length of stay (Level 1+).Sedation protocols that target specific levels of alertness mayreduce duration of IMVand ICU length of stay (Level 1+).Recommendation18. Sedation should be titrated to a specific level of alertness(Grade B).

Patient–ventilator asynchronyPatient–ventilator asynchrony is common and increases patientdiscomfort, the work of breathing, the need for sedation, theincidence of confusion, the need for tracheostomy and the mor-tality rate.132 133 The commonest cause is ineffective triggeringdue to either respiratory muscle weakness and/or excessiveeffort required to overcome iPEEP and trigger a breath.134

Trigger failure is more common during sleep and more likely ifhypercapnia persists by day. A hybrid mode, such as PS with amandatory backup rate is recommended in these circumstancesto avoid pCO2 increasing during sleep.

Auto triggering refers to inappropriately delivered breathsbeing provided by the ventilator. It can be provoked by patientmovement, suctioning, coughing and swallowing, and is morelikely when the trigger sensitivity is set too high. Both a delay inthe onset of a triggered breath or an inadequate amount of PSto sufficiently augment inspiratory flow can lead to an unpleas-ant sensation best described as ‘air hunger’. This can be difficultto detect or for the patient to report. Experienced NIV practi-tioners may trial increasing trigger sensitivity and/or PS, and

monitor the effect on patient comfort and RR. If inadequate PSis given, the breathing rate will fall. The detection of the moresubtle forms of patient–ventilator asynchrony requires examin-ation of the pressure/flow waveforms.135 The most sensitivemeasure of patient–ventilator asynchrony is by simultaneousrecordings of diaphragm electrical activity and pressure changesin the oesophagus.134 Flow rather than pressure triggers reducethe incidence of asynchrony,136 137 as has the move away fromvolume-controlled ventilation.138 139

Proportional assist ventilation (PAV) and neurally adjustedventilatory assist (NAVA) are modes that are being assessed asways to reduce patient–ventilator asynchrony. With PAV, thedegree of pressure support is determined, on a breath by breathbasis, by the patient’s inspiratory effort.140–142 Compared withPS, PAV has been reported to reduce the probability of returningto a controlled mode and the incidence of patient–ventilatorasynchrony.143 In NAVA, the ventilator attempts to match neuraldrive by adjusting the degree of PS (within safe limits), using theelectrical activity of the diaphragm to ‘drive’ the ventilator.Studies comparing patient–ventilator interaction show a reduc-tion in triggering delay with NAVA, reduced cycling delay and areduction in asynchrony events.144 145 Uncertainties persist onhow to adjust the NAVA level and this technical issue is currentlyfrustrating efforts to demonstrate clinical benefit.

It is important to emphasise that patient ventilator asynchronyis common with NIV. While the same principles apply it hasbeen less frequently recognised or investigated. It can criticallyaffect the success of NIV and the patient experience (see below).Evidence statementsPatient–ventilator asynchrony is common and deleterious, andcan be minimised through informed adjustment of ventilatorsettings (Level 2+).Proportional and NAVA have been shown experimentally toreduce ventilator asynchrony but have yet to improve patientoutcome (Level 2+).Recommendations19. Ventilator asynchrony should be considered in all agitatedpatients (including NIV) (Grade C).20. As patients recover from AHRF, ventilator requirementschange and ventilator settings should be reviewed regularly(Grade C).

Use and timing of a tracheostomyIt is accepted that translaryngeal intubation beyond 10 days canbe detrimental.146 147 Historically, it was believed that earlytracheostomy reduced ventilator time and ICU length of stay.148

A survey of ICU physicians in 2005 found that 61% of respon-dents would perform a tracheostomy without first performing atrial of extubation and 50% favoured tracheostomy insertionwithin the first week.149 Two large multicentre studies havefailed to show benefit from tracheostomy performed within7 days of admission.150 151 A subsequent meta-analysis alsoreported no effect on the incidence of ventilator-associatedpneumonia or mortality,152 although less sedation was requiredafter a tracheostomy had been inserted. Tracheostomy carries amorbidity and mortality risk at the time of insertion153 and sub-sequently.154 A UK national report has highlighted the risk ofcritical airway incidents in patients with tracheostomies.155

Accordingly, consideration of the risk and benefit should beundertaken before proceeding to insert a tracheostomy and dueconsideration should be given to using NIV post-extubation toavoid a tracheostomy. This is particularly the case in progressiveNMD/CWD when tracheostomy insertion carries the risk ofpermanence. These aspects, and the evidence summarised


BTS guidelines




below, are considered further in Management of hypercapnicrespiratory failure section.Evidence statementEarly insertion of a tracheostomy does not reduce mortality,duration of IMV, or the incidence of ventilator-associated pneu-monia (Level 1++).Recommendations21. Performing routine tracheostomy within 7 days of initiatingIMV is not recommended (Grade A).22. The need for and timing of a tracheostomy should be indivi-dualised (Grade D).Good practice points▸ In AHRF due to COPD, and in many patients with NMD or

OHS, NIV-supported extubation should be employed inpreference to inserting a tracheostomy.

▸ In AHRF due to NMD, alongside discussion with the patientand carers, the decision to perform tracheostomy should bemultidisciplinary and should involve discussion with a homeventilation unit.

MANAGEMENT OF AHRFObstructive lung diseasesAcute exacerbations of COPD account for 100 000 admissionsannually in England. Of these, around 20% will present with ordevelop hypercapnia,2 7 an indicator of increased risk ofdeath.2 59 The development of AHRF is often multifactorial.These include infection, mucosal oedema, bronchospasm,sputum retention, excessive O2 therapy, sedation, pneumo-thorax, PE and left ventricular failure. Since the publication ofthe BTS guideline in 20021 and subsequent National Institutefor Health and Care Excellence (NICE) recommendations,48 theuse of NIV in AECOPD has increased and most hospitals admit-ting unselected medical patients are able to provide an NIVservice.60

Prevention of AHRF in AECOPDThere is compelling evidence that uncontrolled oxygen therapyincreases the degree of acidosis and subsequent mortality inAECOPD.2 156 In a trial comparing the use of high concentra-tion oxygen versus titrated oxygen in 405 individuals with pre-sumed AECOPD in the pre-hospital (ambulance/paramedic)setting, Austin et al61 reported that titrated oxygen reducedmortality by 58% for all patients (relative risk 0.4) and by 78%for patients with confirmed COPD (RR 0.22). Patients withCOPD who had received titrated oxygen according to theprotocol (targeted at a saturation of 88–92%) were less likely tohave respiratory acidosis (mean difference in pH 0.12) thanthose who received high-concentration oxygen. These dataprovide further evidence to titrate oxygen treatment to amodest target saturation in patients with breathlessness and ahistory or clinical likelihood of COPD. Importantly, the mech-anism(s) of oxygen-induced hypercapnia apply, to varyingdegree, in the other causes of AHRF. Accordingly, the sameoxygen saturation target is recommended in the initial manage-ment of all patients at risk of AHRF.Evidence statementThe use of controlled oxygen therapy in individuals withsuspected AECOPD reduces mortality and the frequency andseverity of AHRF (Level 1++).Recommendation23. In AHRF due to AECOPD, controlled oxygentherapy should be used to achieve a target saturation of 88–92%(Grade A).

Good practice pointControlled oxygen therapy should be used to achieve a targetsaturation of 88–92% in ALL causes of AHRF.

Role of NIV in AECOPDThere are three clinical situations in which NIV is recommendedin AECOPD.157 First, the patient with a modest respiratoryacidosis with the aim of preventing deterioration to a pointwhen IMV would conventionally be considered. Second, as analternative to IMV when conventional criteria for IMV are met(lower pH, more distress) with the intention to proceed to IMVif NIV fails. Third, as the ‘ceiling’ of treatment for patientswho, for whatever valid reason, are not candidates for IMV. Theevidence base for NIV has rarely defined the particular patientcase mix in this way.

There have been many trials of NIV in acidotic AECOPD,including 21 where NIV was compared to standard non-ventilatory treatment, one trial of NIV versus sham NIV andtwo trials of NIV versus IMV. Five of the studies were con-ducted in an ICU setting, one in the pre-hospital setting, twoin emergency departments (EDs), two in HDUs and theremainder in general wards. In general, patients in studiesconducted in the ICU had lower pH and therefore moresevere exacerbations.158

In a meta-analysis of NIV use versus usual care, NIV wasassociated with a lower mortality (relative risk 0.41), a lowerneed for intubation (relative risk 0.42), lower likelihood oftreatment failure (relative risk 0.51) greater improvements at1 h in pH (weighted mean difference 0.03), pCO2 (weightedmean difference −0.40 kPa) and RR (weighted mean differ-ence −3.08 breaths/min). NIV also resulted in fewertreatment-associated complications (relative risk 0.32) and ashorter duration of stay in hospital (weighted mean difference−3.24 days).16

In one trial, NIV was compared to IMV for AECOPD after afailure of standard medical treatment. There was no differencein survival. However, in those patients in whom NIV was suc-cessful, duration of hospital stay was shorter, there were fewercomplications, fewer patients required de novo oxygen supple-mentation and there were fewer readmissions to hospital in thefollowing year.158

No trial has demonstrated a worse outcome with NIV com-pared to non-ventilatory management, although, in one study,NIV use may have caused a delay in escalation to IMV.159 Thedanger that the use of NIV may inadvertently lead to a worseoutcome is, however, suggested by a large American retrospectivestudy. Chandra et al160 reported on an estimated 7.5 millionadmissions for AECOPD in the USA between 1998 and 2008.During this period, there was a 460% increase in the use of NIVand a 42% decline in IMV use. Worryingly, given the increasingfamiliarity of staff using NIV over time, the number of patientsfailing NIV and requiring IMV increased as did hospital mortal-ity. By 2008, NIV failures had a 29% risk of death, a 60% greaterrisk than patients managed by immediate intubation and provi-sion of IMV. NIV failures, who were then managed by IMV, had asevenfold greater risk of death than patients successfully treatedby NIV. Possible explanations include the fact that further physio-logical deterioration may have resulted from the delay in theinstitution of IMV in NIV failures and/or that patients who failNIVare more severely ill.161

The outcomes in AECOPD reported in the UK NationalCOPD Resources and Outcomes project (NCROP)7 are also ofconcern, as NIV outcome was less favourable than reported inthe RCTs discussed above. The low level of ICU involvement


BTS guidelines




and/or use of IMV reported has led to the suggestions that theclinical environment in which NIV was delivered was inad-equate for the level of patient complexity/acid–base disturbance,that there was an over-reliance on the effectiveness of NIV andan under recognition of NIV failure.7 Similar conclusions can bedrawn from BTS NIV audits. In the most recent survey, carriedout in 2013, median pH was 7.24 and yet NIV was providedoutside of HDU/ICU in 91%. In the AECOPD group (61% ofAHRF cases), overall mortality was 28% in those admitted toHDU/ICU and 40% for those admitted to admission wards.5

See Care planning and delivery of care section for furtherconsideration of the possible unintended consequences of theintroduction of NIV in managing AHRF.

In around 20% of AHRF cases secondary to AECOPD, opti-mised medical therapy, which includes targeting an oxygen sat-uration to 88–92%, will result in normalisation of arterialpH.2 62 Established guidance is therefore to await improvementand initiate NIV if, after 60 min, the following are present: pH<7.35, pCO2 > 6.5 kPa and RR >23 breaths/min.1 48

There is some evidence that NIV may also be beneficial inpatients with hypercapnia in the absence of acidosis. A studyfrom China162 showed a reduction in the need for endotrachealintubation in a subgroup analysis of patients with hypercapniabut a pH >7.35 (9/80 vs 2/71, p=0.04). However, length ofstay and duration of NIV were longer than in a similar UKstudy,163 and there was a high incidence of side effects, particu-larly gastric distension (23%), despite low inflation pressurebeing used (IPAP 12±4). It is unclear if this study is applicableto UK practice.

There is insufficient evidence to support the use of absolutevalues of pH or pCO2 as an indication for IMV rather thanNIV.164 Nevertheless, a pH of 7.25 has been suggested as athreshold level below which IMV should be considered. NIVmay still be effective at reversing such severe acidosis but thefailure rate is higher.158

Evidence statementsOptimal medical therapy, including controlled oxygen therapy,leads to a resolution of respiratory acidosis in 20% of indivi-duals with AECOPD (Level 1+).Compared with standard medical therapy, NIV improves sur-vival, reduces the need for endotracheal intubation, reducescomplications and reduces length of stay (Level 1+).There is no lower limit of pH below which a trial of NIV hasbeen shown to be harmful (Level 2++).Continued use of NIV when the patient is deteriorating, ratherthan escalating to IMV, increases mortality (Level 2+).Audit data show that ‘real world’ outcomes do not reproducethose demonstrated in the RCTs (Level 2+).One risk of an expansion of ward-based rather then HDU/ICUprovision of NIV may be greater delay in expert review and/orescalation to IMV (Level 4).Recommendations24. For most patients with AECOPD, the initial managementshould be optimal medical therapy and targeting an oxygen sat-uration of 88–92% (Grade A).25. NIV should be started when pH<7.35 and pCO2>6.5 kPapersist or develop despite optimal medical therapy (Grade A).26. Severe acidosis alone does not preclude a trial of NIV in anappropriate area with ready access to staff who can perform safeendotracheal intubation (Grade B).27. The use of NIV should not delay escalation to IMV whenthis is more appropriate (Grade C).28. The practice of NIV should be audited regularly to maintainstandards (Grade C).

Starting NIV in COPDRecommendations regarding investigations before starting NIVare based on expert opinion. ABG measurement is required todiagnose and quantify the severity of AHRF, and a chest radio-graph is needed to seek evidence of causation or complications.To avoid any delay in giving ventilatory support, NIV should beinitiated in extreme acidosis (pH<7.25) without waiting for achest X-ray. Other investigations (eg, full blood count (FBC), U+E, ECG) should be performed and treatment directed at anyreversible factors contributing to AHRF. In some cases, echocar-diography may be indicated to exclude acute pulmonaryoedema. As is further discussed in Care planning and deliveryof care section, it is recommended that an action plan be agreedin the event of NIV failure and that this is documented at thestart of treatment.Good practice points▸ ABG measurement is needed prior to and following starting

NIV.▸ Chest radiography is recommended but should not delay ini-

tiation of NIV in severe acidosis.▸ Reversible causes for respiratory failure should be sought and

treated appropriately.▸ At the start of treatment, an individualised patient plan

(involving the patient whenever possible) should documentagreed measures to be taken in the event of NIV failure.

Prognostic features relating to use of NIV in COPDThe 2003 UK National COPD audit165 demonstrated a higherhospital mortality in patients with a lower admission pH andoxygen saturation, higher urea, lower albumin and older age(see below for further discussion), irrespective of treatmentmodality. Increased base excess (indicating chronicity of hyper-capnia), MRC dyspnoea index and RR are additional prognosticvariables.165 166 The presence of pulmonary consolidation onX-ray and impaired consciousness level (GCS<8) increase theNIV failure rate,167 although successful outcome despiteimpaired consciousness has been reported.49 168

In contrast, Nava et al169 reported a good outcome forpatients aged >75 years, in terms of intubation avoidance andreduced mortality with NIV. Others have also achieved satisfac-tory results in the elderly.170 However, in a retrospective ana-lysis of 240 ward-based cases from a single centre, age>75 years was associated with poorer outcomes with NIV.171

The NCROP audit, which collected data on 9716 AECOPDadmissions, reported mortality at 12% when the presentationpH was the lowest value reached, 24% when acidosis increasedafter presentation and 33% when acidosis only developed afteradmission.7 These findings reflect a combination of increasingseverity of illness and a lack of response to standard medicaltreatment. In addition, delay in providing therapeutic NIV and/or IMV contributed. The audit also highlighted that a coinci-dent metabolic acidosis was an adverse finding.

Once NIV has been initiated, a reduction in RR and improve-ment in pH within 4 h predicts NIV success.172 Associated fea-tures are a reduction in signs of respiratory distress, reducedanxiety or agitation and a decrease in heart rate. In one largestudy, Confalonieri et al173 showed that, if pH <7.25 and RR>35 persist, NIV failure is likely. Worsening acidosis, afterinitial improvement with NIV, is also associated with a worseprognosis.174–176 In a case series published by Moretti et al,20% of patients deteriorated after initially improving with NIV.In these circumstances, prognosis was poor whether patientswere subsequently intubated or continued with NIV.177


BTS guidelines




Roche Campo et al93 found that polysomnographic evidenceof severe sleep disturbance in patients with COPD with AHRFcorrelated with a poor outcome and Gursel et al,91 reporting ona retrospective analysis of patients with COPD and OHS treatedin an ICU setting, found better outcome in patients receivingpressure control rather than overnight PS. Clinical research instable sleep hypoventilation also suggests that limiting theincrease in hypercapnia during sleep is important and that acontrolled ventilation mode may be more advantageous than theassist mode.178

Evidence statementsAdvanced age is not an important determinant of outcome withNIV treatment of AHRF (Level 1+).An improvement in physiological parameters, usually within 1–2 h, particularly pH and RR, predict a successful outcome fromNIV treatment (Level 1+).Worsening of physiological parameters, particularly pH and RR,is predictive of an increased risk of death and/or requirementfor intubation (Level 1+).Recommendations29. Advanced age alone should not preclude a trial of NIV(Grade A).30. Worsening physiological parameters, particularly pH andRR, indicate the need to change the management strategy. Thisincludes clinical review, change of interface, adjustment of venti-lator settings and considering proceeding to endotracheal intub-ation (Grade A).Good practice pointIf sleep-disordered breathing pre-dates AHRF, or evidence of itcomplicates an episode, the use of a controlled mode of NIVovernight is recommended.

Duration of NIV in COPDNormalisation of pH and a pCO2 <6.5 are commonly used as aguide to the discontinuation of NIV. Restoring respiratory drivewill require a prolonged period of NIV to reduce the pCO2

than to correct the acidosis.The optimal amount of NIV in the initial period, and the

most effective way to withdraw it as the patient improves, havenot been examined in published trials. As the work of breathingfalls and acute hyperinflation reverses, as a result of treatmentwith steroids, antibiotics and intense broncholdilator therapy,unsupported alveolar ventilation will return towards normal.The more florid the evidence for infection precipitating AHRF,the more likely there is to be full reversal. Normalisation ofpCO2 may not be possible in some patients, particularly thosewho show evidence of chronic hypercapnia at presentation.

In most RCTs, the intention has been that patients shouldreceive semicontinuous NIV for the first 24 h. The amount ofNIV actually delivered, when this has been reported, has beenless than planned, from a median of 20 h in one study179 to 7 hin another.163 Conventional practice is to gradually reduce theamount of time on NIV, with increasingly prolonged periods ofself-ventilation during the day, while continuing with NIV over-night. Monitoring of pCO2 on and off NIV is a useful guide tohow quickly the withdrawal of NIV can proceed.Transcutaneous pCO2 measurement may facilitate this betterthan continuing with arterial or capillary sampling. A gradualreduction of ventilator pressures, and a switch to PS or a reduc-tion in backup rate, should mirror patient recovery. Attempts toadjust ventilator settings to achieve patient comfort remainimportant. Those with a less clear infective cause for AHRF,and/or evidence of chronicity of hypercapnia, should be assessedfor alternative or additional causative factors such as marked

fluid retention, obstructive sleep apnoea (OSA) or OHS. Onestudy suggested there may be an advantage to employing NIVfor longer than the conventional 3 days.162 More trial data areneeded to guide optimal withdrawal of NIV.Evidence statementIn clinical trials, NIV has been discontinued when there hasbeen normalisation of pH and pCO2 and a general improve-ment in the patient’s condition (Level 1+).Recommendation31. NIV can be discontinued when there has been normalisationof pH and pCO2 and a general improvement in the patient’scondition (Grade B).Good practice points▸ Time on NIV should be maximised in the first 24 h depend-

ing on patient tolerance and/or complications.▸ NIV use during the day can be tapered in the following 2–

3 days, depending on pCO2 self-ventilating, before being dis-continued overnight.

Optimising NIV delivery and technical considerationsThe commonest reasons for failure of NIV are excessive maskleak, insufficient PS and ventilator patient asynchrony. If the PSis inadequate, alveolar ventilation will not be significantlyincreased. This may be detected by a lack of augmentation ofchest and abdominal wall movement. National NIV audits haverevealed that inadequate IPAP is often used in AECOPD.3 4 Ingeneral, while a patient might be started on NIV with an IPAPof 15, this should be progressively increased to reach an IPAP of20–30 within 10–30 min, the need for higher pressure and amore rapid escalation being indicated by patient size and moresevere acidosis, respectively.

In the presence of persisting hypoxaemia, that is thoughtunrelated to sputum retention, the EPAP may need to beincreased in an attempt to recruit areas of poorly ventilatedlung. (It may also be appropriate if there is a degree of upperairway obstruction). If ineffective, or if this results in distress,senior review is indicated while the FiO2 is temporarilyincreased.

Leak should always be minimised by mask adjustment and/orby changing the mask type. Positional upper airway obstructionmay result in ineffective NIV. It is often indicated by variablemask leak. Care is needed to ensure head flexion is avoided,

Table 3 Technical issues: a guide for when NIV is failing

Problem Cause(s) Solution (s)

Ventilator cyclingindependently of patienteffort

Inspiratory triggersensitivity is toohighExcessive mask leak

Adjust triggerReduce mask leak

Ventilator not triggeringdespite visible patient effort

Excessive mask leakInspiratory triggersensitivity too low

Reduce mask leakAdjust triggerFor NM patients considerswitch to PCV

Inadequate chest expansiondespite apparent triggering

Inadequate Tidalvolume

Increase IPAP. In NM orchest wall diseaseconsider longer Ti

Chest/abdominal paradox Upper airwayobstruction

Avoid neck flexionIncrease EPAP

Premature expiratory effortby patient

Excessive Ti or IPAP Adjust as necessary

EPAP, expiratory positive airway pressure; IPAP, inspiratory positive airway pressure;NIV, non-invasive ventilation; NM, neuromuscular; PCV, pressure-controlledventilation.


BTS guidelines




particularly in sleep. Patient–ventilator asynchrony may becaused by mask leak, insufficient or excessive IPAP, inappropriatesetting of Ti or Te, high levels of intrinsic PEEP or excessivelysensitive triggers. If the cause is unclear, advice should besought from an experienced NIV practitioner.

Although there is no agreed definition of NIV failure, it is sug-gested by persisting or worsening of acidosis despite attempts tooptimise NIV delivery. In these circumstances, further adviceshould be sought as soon as possible. NIV failure is associatedwith low/falling pH172 and a high APACHE II score.180 Persistingwith ineffective NIV adds to patient discomfort and, if IMV isindicated, risks further patient deterioration and cardiorespira-tory arrest. Evidence that this risk is real comes from the use ofNIV in post-extubation respiratory failure where delay inre-intubation, caused by persisting with NIV when ineffective,increased mortality.181 If NIV is adding to patient distress, andintubation has been deemed to be inappropriate (see below), NIVshould be discontinued and palliative care measures adopted.Good practice pointBefore considering NIV to have failed, check that common tech-nical issues have been addressed and ventilator settings are optimal.

Indications for IMV in AECOPDIntubation should be immediately considered for patients pre-senting with or developing respiratory arrest, gasping respiration,a pH <7.15 or showing signs of a low cardiac output. Intubationmay also be appropriate if NIV is contra-indicated or technicallyimpossible and when NIV has been tried but has failed.

There is insufficient evidence to support the use of absolutevalues of pH or pCO2 as intubation criteria and it is unlikelythat any absolute value would be applicable to all patients in allsituations.164 Nevertheless, pH<7.25 has been suggested as alevel below which IMV should be considered and <7.15 as thelevel that IMV is indicated (following initial resuscitation anduse of controlled oxygen).

In the UK, only a small proportion of patients receiving NIVtreatment escalate to IMV despite data suggesting more shoulddo so.3 4 7 A degree of unjustified ‘therapeutic nihilism’ mayhave shaped UK IMV practice. Duration of ICU stay and sur-vival in AECOPD is better than most other medical causes forwhich invasive ventilation is employed.6 In a prospective cohortstudy, clinicians’ estimated prognosis for patients with AECOPDor chronic asthma was lower than indicated by predictivemodelling.182

Specialist support to staff providing NIV may reduce mortal-ity. In one study, employing critical care outreach nurses, themortality was reduced from 57% to 35%. This was in part dueto a greater number of patients receiving IMV.183 Validatedprognostic scoring tools (see next section) may aid discussionregarding intubation. Box 1 summarises the indications for IMVin AECOPD.Evidence statementsIntubation is indicated if NIV is failing (unless it is agreed thatthis is not desired by the patient or it is deemed not in thepatient’s ‘best interest’) (Level 1+).Neither patient characteristics nor pathophysiological para-meters are sufficiently robust to predict the success of NIV orIMV but, in general, the more adverse features that are presentand the greater the physiological disturbance the higher thechance of treatment failure or death (Level 2++).Recommendations32. IMV should be considered if there is persistent or deterior-ating acidosis despite attempts to optimise delivery of NIV(Grade A).

33. Intubation should be performed in respiratory arrest or peri-arrest unless there is rapid recovery from manual ventilation/provision of NIV (Grade D).34. Intubation is indicated in management of AHRF when it isimpossible to fit/use a non-invasive interface, for example,severe facial deformity, fixed upper airway obstruction, facialburns (Grade D).35. Intubation is indicated where risk/benefit analysis by anexperienced clinician favours a better outcome with IMV thanwith NIV (Grade D).

Outcome following NIV or IMV in AECOPDThere are a number of tools that may inform discussion regard-ing prognosis in COPD. Some were developed for use in thestable setting, such as the BODE index184 and the DECAFscore.185 APACHE II, a generic acute physiology score, wasdeveloped using parameters available at ICU admission. Despitebeing generic, it retains predictive value of mortality inAECOPD.180 186 187 Wildman et al188 analysed a large UK ICUclinical database (with a 35% mortality) to develop a disease-specific score, the COPD and Asthma Physiology Score (CAPS).This was based on 8, mainly biochemical, variables. CAPS wasreported to perform better than generic scoring. The authorsacknowledge that normal functional assessment, for example, bybody mass index (BMI), usual functional status and presence ofcomorbidity, might improve predictive power.

Confalonieri et al189 suggested that prognosis following suc-cessful use of NIV in AHRF was better than if IMV wereemployed. The number and length of further hospitalisationswere significantly higher and the survival rate at 12 months sig-nificantly lower (50% vs 71%) than in patients who receivedNIV. Follow-up of patients in the RCT of Plant et al172 showeda median survival of 16.8 months in those treated with NIV and13.4 months in those receiving standard treatment (p=0.12).The trend in improved survival was attributable to preventionof death during the index admission.

A study of an inception cohort of 73 106 patients withCOPD, followed up after their first AHRF treated by NIV,reported a 2-year survival of 70% and a median survival of 3.6years.190 After a second hospitalisation, patients typicallyentered a deteriorating pattern with more frequent and severeepisodes until death. A retrospective analysis of 100 patientswith COPD, followed for up to 5 years after their first episodeof NIV,191 found that 52% survived 2 years. When the BMI was<22 kg/m2, age >75 years or there was prior home oxygen use,survival was only 26%. In a prospective cohort of patients withCOPD surviving AHRF treated by NIV,192 80% werere-admitted within a year, of whom 50% died. APACHE IIscore at admission, home oxygen prescription and a BMI below25 predicted early recurrent AHRF or death.

Box 1 Indications for invasive mechanical ventilation(IMV) in acute exacerbation of COPD (AECOPD)

▸ Imminent respiratory arrest▸ Severe respiratory distress▸ Failure of or contra-indications to non-invasive ventilation

(NIV)▸ Persisting pH<7.15 or deterioration in pH despite NIV▸ Depressed consciousness (Glasgow Coma Score <8)


BTS guidelines




In summary, an admission with AHRF is a critical point in thenatural history of COPD, with a more accelerated decline in mostpatients following recovery. It indicates a high risk of recurrence ofAHRF and poor long-term prognosis. Survival data vary betweenpublished studies, presumably a reflection of differences in casemix. Survival might be better if NIV is successfully employed forAHRF than if IMV is used. An important management point is thatthe first episode of AHRF should prompt a discussion about life-style, patient wishes for management of future episodes and discus-sions about end-of-life care generally.

There is evidence of ‘prognostic pessimism’ among clinicianscaring for patients with AECOPD. In an outcome study of 517patients, 62% survived to 180 days, yet overall predicted survivalat the time of admission was 49%.182 For those considered to bein the worst prognostic group (a survival rate of 10%), 40% recov-ered. Accordingly, as survival from AECOPD becomes less likely,clinicians become worse at prediction and err on the side of under-estimating survival. By implication, it is likely that patients whomight otherwise survive are currently being denied admission toICU because their survival potential is underestimated.Importantly, from a patient perspective, Wildman et al193 reportedthat the majority of patients surviving IMV for AHRF had stableand acceptable QoL despite poor health status and 96% statedthey would opt for IMVagain under similar circumstances.Evidence statementThere are validated tools for the assessment of prognosis instable and exacerbating COPD populations but, on their own,they are unreliable for individual prognostication (Level 2++).Physicians underestimate survival potential in AECOPD treatedby IMV (Level 2+).The majority of patients with COPD or chronic asthma whoreceive IMV would elect to receive it again (Level 2+).An episode requiring ventilatory support generally indicatesadvanced disease with a high risk for future episodes of AHRFand a limited prognosis (Level 2++).Recommendations36. Prognostic tools may be helpful to inform discussion regard-ing prognosis and the appropriateness of IMV with the caveatthat such tools are poorly predictive for individual patient use(Grade B).37. Clinicians should be aware that they are likely to underesti-mate survival in AECOPD treated by IMV (Grade B).38. Clinicians should discuss management of possible future epi-sodes of AHRF with patients following an epsiode requiringventilatory support because there is a high risk of recurrence(Grade B).

Acute asthmaFive small RCTs194–198 of NIV in acute asthma have been pub-lished. Four were conducted in the ED and one in a respiratoryICU. Importantly, none of the RCTs included patients withhypercapnia and intubation rates were low.199 Most showedtreatment with NIV led to a faster improvement in FEV1 and ashorter ICU/hospital stay. They all have important design weak-nesses. The trial by Soma et al197 lacked a second control arm(conventional inhaled bronchodilators) and the trial by Brandaoet al194 did not give systemic steroids. No information was pro-vided about acceptability of NIV to patients. The only studyreporting use in AHRF asthma was a retrospective cohort studyby Meduri et al200 of 17 patients with a mean pH of 7.25. NIVwas reported to be successful in avoiding intubation in 15.

The use of NIV in acute asthma, particularly AHRF, needs tobe set in the context of a very low mortality rate with IMV.201

There is also the potential for patients with acute asthma to

deteriorate rapidly, to require high inflation pressures and a highinspired oxygen concentration. Trialling NIV therefore carriessignificant risk. The patient with brittle asthma or a very shorthistory suggesting hyperacute brochospasm, especially whenoxygen toxicity in transit is implicated, might justify a trial ofNIV in the resucitation area but, in all other circumstances, ven-tilatory support should be by intubation and provision of IMV.The overall invasive management of acute severe asthma issimilar to that in AECOPD but a higher SaO2 target of 96% isadvised. For more specialist consideration, the reader is referredto standard textbooks or recent reviews.

Acute (and chronic) hypercapnia may complicate chronicasthma, a condition that shares many features of COPD, such aschronic hyperinflation, persistent and only partially reversibleairflow obstruction, mucus hypersecretion and infective exacer-bations. As the pathophysiology is similar, the guidance on theuse of NIV and IMV in AECOPD applies to the chronic asth-matic with AHRF.Evidence statementsThere is insufficient evidence to support the use of NIV inAHRF in acute asthma (Level 3).IMV in acute asthma carries a very low mortality rate. Mostasthma deaths relate to presentation in extremis or a failure toimmediately implement IMV when indicated rather than afailure of IMV per se (Level 2+).Recommendations39. NIV should not be used in patients with acute asthmaexacerbations and AHRF (Grade C).40. Acute (or acute on chronic) episodes of hypercapnia maycomplicate chronic asthma. This condition closely resemblesCOPD and should be managed as such (Grade D).

Non-CF bronchiectasisRecurrent episodes of hypercapnic respiratory failure may char-acterise bronchiectasis with periods of good or acceptablequality of life (QoL)/health status in the intervening months oryears. In some, domiciliary ventilation will be indicated forsymptoms of sleep disordered breathing. There are no RCTs ofNIV versus IMV in acute exacerbations of bronchiectasis. Therecommendations regarding NIV for AECOPD are appropriatealthough there is the additional challenge of excessive and diffi-cult to clear sputum. NIV may relieve breathlessness and helppatients to participate more effectively with physiotherapy. Amini-tracheostomy, or other techniques to aid sputum clearance,may be indicated.202

There is scant data on outcomes for AHRF in non-CF bron-chiectasis. In a retrospective review203 of patients managed byNIV (n=31) or IMV (n=26) for AHRF, the NIV group had lesssevere physiological disturbance. There was no difference inhospital mortality between the two groups (26% and 27%). TheNIV failure rate (need for intubation, or death in the ICU) was33%. Using logistic regression, the APACHE II score was theonly predictor of hospital mortality (OR 1.19 per point) andthe severity of hypoxia (pO2/FiO2 ratio) the only predictor ofNIV failure (OR 1.02/mm Hg decrease). Hospital mortality ofpatients with AHRF secondary to bronchiectasis is thereforeapproximately 25% whether management is by NIV or IMV.When selectively applied, NIV fails in one-third and this is pre-dicted by the degree of hypoxaemia. Similar criteria should beused as in AECOPD when deciding appropriateness of intub-ation: health status, comorbidities, previous episodes of IMVand patient preferences. Evidence of an acute precipitatingfactor (infection) should favour intubation, as reversibility ismore likely than in progressive chronic hypercapnia.


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Evidence statementsIn non-CF bronchiectasis and AHRF, NIV is indicated if there isrespiratory acidosis using the same criteria as in AECOPD(Level 3).Outcome with NIV is no worse than with IMV in selectedpatients (Level 2+).Recommendations41. In patients with non-CF bronchiectasis and AHRF, con-trolled oxygen therapy should be used (Grade D).42. In patients with non-CF bronchiectasis, NIV should be startedin AHRF using the same criteria as in AECOPD (Grade B).43. In patients with non-CF bronchiectasis, NIV should usuallybe tried before resorting to IMV in those with less severephysiological disturbance (Grade C).44. In non-CF bronchiectasis, the patient’s clinical conditionprior to the episode of AHRF, and the reason for the acutedeterioration, should be evaluated and used to inform the deci-sion about providing IMV (Grade C).Good practice points▸ In patients with non-CF bronchiectasis, the precipitating

cause is important in determining short-term prognosis.▸ Health status prior to the episode of AHRF is an important

predictor of outcome.

Cystic fibrosisRecurrent episodes of acute on chronic hypercapnic respiratoryfailure characterise advanced CF, such episodes usually beingpreciptated by infection. There may be intervening months ofacceptable QoL/health status. There are no RCTs of NIV versusIMV in AHRF and the recommendations regarding NIV forAECOPD remain appropriate. Hypoxaemia is often more severethan in AECOPD, in some, relating to co-existent pulmonaryhypertension. Secretion clearance is also a major issue and mayrender NIV ineffective or poorly tolerated.204–207 Case series ofpatients with CF receiving NIV as a bridge to transplantationhave been reported.208 209

As the outcome of invasive ventilation in CF is generallypoor, it has been recommended that NIV be used preferen-tially.202 In a retrospective multicentre study of 60 ICU hospita-lisations for 42 adult patients with CF admitted between 2000and 2003, NIV was used in 57% and was successful in 67% ofthese.210 Endotracheal intubation was implemented on 19 occa-sions and ICU mortality was 14%. Among recognised markersof CF disease severity, only the annual FEV1 loss significantlyrelated to outcome (HR=1.47, p=0.001). Admission SAPS II, apathophysiological score, weakly predicted outcome (HR=1.08,p<0.001), but the perceived need for endotracheal intubationstrongly predicted mortality (HR=16.60, p<0.001). In a studyfrom a single centre, 30 patients were managed by IMV on 34occasions.211 Eleven patients died in the ICU and a furtherseven before hospital discharge. Sixty per cent intubated forpneumothorax and/or haemoptysis survived contrasting, withonly 30% when intubated for infection. Mean survival post-discharge was 447 days. There were no significant differences insurvivors for colonising organism, frequency of infective exacer-bations or acute severity of illness. A greater fall in BMI overthe preceding 24 months was more frequent in non-survivors.The authors concluded that patients with CF developing AHRFdue to haemoptysis and/or pneumothorax should be consideredfor management by IMV.Evidence statementsChronic disease markers are more relevant than rates of hospi-talisation or FEV1 decline in assessing outcome in AHRF com-plicating CF (Level 2+).

When ventilatory support is needed, outcome following IMV isworse than with NIV, especially when infection is the precipitant(Level 2+).Secretion clearance is a major issue and may render NIV inef-fective or poorly tolerated (Level 2−).Recommendations45. In patients with CF, controlled oxygen therapy should beused in AHRF (Grade D).46. In patients with CF, NIV is the treatment of choice whenventilatory support is needed (Grade C).47. In patients with CF, specialised physiotherapy is needed toaid sputum clearance (Grade D).48. In patients with CF, a mini-tracheostomy combined withNIV may offer greater chance of survival than resorting to IMV(Grade D).

Restrictive lung diseaseThe causes of AHRF include severe chest wall deformity, neuro-muscular conditions that affect the respiratory muscles andOHS. Presentation is often with advanced chronic hypercapnia.An insidious decline in health may not have been medicallyrecognised as being due to the development of respiratoryfailure. Acute presentations, often with infection precipitatingacute illness, are likely when the VC is <1 L. Unlike AECOPD,recurrent critical episodes do not preclude intervening good lifequality, acceptable health status and prolonged survival. Thereare no RCTs to guide practice in AHRF and the recommenda-tions presented are extrapolated from the AECOPD literature,from reports of the value of domiciliary NIV (most evidencecoming from trials in the more progressive NMDs) and fromexpert opinion.

NMD and CWDRespiratory impairment generally parallels disease progressionin NMD. However, in some, diaphragm involvement precedeslocomotor disability and presentation with acute on chronichypercapnia is typical. This pattern is characteristic of acidmaltase deficiency and the amyotrophic lateral sclerosis varietyof motor neurone disease. In some of the muscular dystrophies,bulbar muscle involvement is common. As a result, sleep disor-dered breathing may arise from a combination of respiratorymuscle weakness and upper airway obstruction. The resultingnocturnal hypoventilation will then gradually spill over intodaytime hypercapnia. Bulbar dysfunction also renders voluntarycough less effective. NICE had previously published guidanceon the use of NIV in motor neurone disease,212 which did notconsider management of acute illness nor the value of intub-ation if NIV fails. New guidance from NICE on motor neuronedisease is in preparation. While respiratory failure is predictablein the majority, some MND patients present before a formaldiagnosis has been made.213 214 This also occurs in less progres-sive conditions such as Limb Girdle muscular dystrophy orMyotonic Dystrophy. Without domicilary NIV, the naturalhistory of neuromuscular and CWDs is of progressive chronichypercapnic failure leading to death. It is well recognised suchindividuals can survive long term on home NIV with a goodQoL, even if they present initially in severe respiratory failure.Thus individuals with NMD and CWD who present withAHRF should not be denied acute NIV. The success of domici-lary NIV has made the management of any associated cardiomy-opathy increasingly clinically relevant.

In CWD, evidence of pre-existing sleep disordered breathingis also common at AHRF presentation. In some, markedchronic hypercapnia is an unexpected finding when ABGs are


BTS guidelines




performed. Such patients may have established pulmonaryhypertension, chronic hypoxaemia and polycythaemia.

In contrast to AECOPD, where the degree of acidosis is moreimportant than the degree of hypercapnia, any elevation ofpCO2 in NMD/CWD may herald an impending crisis.213

Patients have a reduced respiratory reserve but may initiallysustain sufficient alveolar ventilation to maintain normal carbondioxide tension. Minor infection, such as coryza, may be pro-vocative and over the next 24–72 h progressive hypercapniamay develop. Tolerance of acute and chronic hypercapnia variesconsiderably. Some patients are excessively sleepy with minimalelevation of pCO2, while others remain alert despite muchmore severe hypercapnia. NIV should be considered in anybreathless/acutely unwell patient with NMD/CWD beforerespiratory acidosis develops.

In the absence of bulbar dysfunction, NIV is usually well tol-erated in the restrictive causes of AHRF. Unless there is signifi-cant skeletal deformity, a low degree of PS (eg, a pressuredifference of 8–12 cm) is needed in NMD. By contrast, insevere kyphoscoliosis, an IPAP >20, and sometimes up to 30,may be required because of the high impedance to inflation.Expiratory flow is normally not limited in either restrictive cat-egory and the inspiratory/expiratory time (IE) ratio for thebackup rate (or PCV) should initially be set at 1:1 to allow anadequate time for inspiration. Bulbar dysfunction renders effect-ive NIV more difficult to achieve, requires a higher EPAP toovercome upper airway obstruction and needs special attentionto aid cough and the clearing of upper and lower airways.Clinical experience in providing NIV is needed to best titratethe EPAP. A modest increase in the domiciliary ventilator set-tings is advised in the case of home mechanical ventilationpatients being admitted with AHRF.

While triggering is usually normal in CWD, it is commonlyinadequate in the other restrictive conditions. Many patientswith NMD find PCV more comfortable and this may also moreeffectively control nocturnal hypoventilation.Evidence statementThere are no trials comparing NIV with IMV in AHRF inNMD or CWD. Domiciliary NIV is effective in treating chronichypercapnia, improves long-term survival and preserves a goodor acceptable QoL (Level 4).Recommendations49. Controlled oxygen therapy should be used in patients withNMD or CWD and AHRF (Grade D).50. NIV should almost always be trialled in the acutely unwellpatient with NMD or CWD with hypercapnia. Do not wait foracidosis to develop (Grade D).51. In patients with NMD or CWD, NIV should be consideredin acute illness when VC is known to be <1 L and RR >20,even if normocapnic (Grade D).52. In patients with NMD or CWD, consider controlled ventila-tion as triggering may be ineffective (Grade D).53. In NMD and CWD, unless escalation to IMV is not desiredby the patient or is deemed to be inappropriate, intubationshould not be delayed if NIV is failing (Grade D).Good practice points▸ Individuals with NMD and CWD who present with AHRF

should not be denied acute NIV.▸ NIV is the ventilation mode of choice because patients with

NMD or CWD tolerate it well and because extubation fromIMV may be difficult.

▸ In patients with NMD or CWD, deterioration may be rapidor sudden, making HDU/ICU placement for therapy moreappropriate.

▸ In patients with NMD or CWD, senior/experienced input isneeded in care planning and is essential if differences inopinion exist or develop between medical staff and patientrepresentatives.

▸ In patients with NMD, it should be anticipated that bulbardysfunction and communication difficulties, if present, willmake NIV delivery difficult and may make it impossible.

▸ Discussion about NIV and IMV, and patients’ wishes withrespect to cardiopulmonary resuscitation, should occur aspart of routine care in patients with NMD or CWD.

▸ In patients with NMD or CWD, nocturnal NIV shouldusually be continued following an episode of AHRF pendingdiscussion with a home ventilation service.

NIV failure and discontinuing NIV following recovery in NMD and CWDDecisions regarding resuscitation and intubation can be particu-larly challenging as little or no evidence exists for most of thecausative conditions, communication with the patient may be diffi-cult and/or cognition be impaired and there may be unreasonableexpectation on the part of families and carers. A resuscitation planis important but may be difficult to negotiate. Inability to clearsecretions is a common cause of NIV failure. This may result froman excessive volume of secretions or from a combination oflimited inspiratory capacity, expiratory muscle weakness andbulbar dysfunction. Specialist advice and experience is required tomanage NIV in the presence of bulbar dysfunction and to provideeffective cough assistance.215 As with all patients, good communi-cation is important. As this may be a challenge, it is another reasonfor seeking specialist help and advice. Enlisting the help of normalcarers may be useful because they may engender more reassuranceto patients and be better at aiding sputum clearance.

Recovery usually takes longer than in AECOPD, so that step-ping down the time on NIV should proceed more slowly, andNIV will need to be continued overnight. The higher the pres-entation HCO3, the longer the period of relative hyperventila-tion required to reduce buffering capacity. A target pCO2

around 6.5 kPa self ventilating is recommended. Followingrecovery, the majority of individuals with NMD or CWD willrequire NIV at home. NIV should continue overnight until dis-cussion with a home ventilation service.Good practice points▸ In patients with NMD or CWD, intolerance of the mask and

severe dyspnoea are less likely to cause NIV failure. Bulbardysfunction makes NIV failure more likely.

▸ Deterioration in patients with NMD or CWD may be verysudden. Difficulty achieving adequate oxygenation or rapiddesaturation during a break from NIV are important warningsigns.

▸ In patients with NMD or CWD, the presence of bulbar dys-function, more profound hypoxaemia or rapid desaturationduring NIV breaks suggests that placement in HDU/ICU isindicated.

IMV in NMD/CWDMany clinicians have limited experience of managing NMD andCWD. There is the danger of underestimating survival potentialin the face of severe general disability. Patient choice and seekingthe views of advocates when communication with the patient isdifficult are paramount. Discussion with a specialist centre onboth the delivery of IMVand weaning is recommended.

The risk of sudden deterioration is greater due to reducedrespiratory reserve, impaired cough, cardiomyopathy (possiblyundiagnosed) and sometimes communication challenges.Intubation practice, elective or in AHRF, varies between centres


BTS guidelines




and between countries. For instance, in motor neurone disease(MND), elective intubation is reported to occur in 0.8%(Ireland), 6% (USA) and 10.6% (Italy) of cases.214

Outcome data following IMV are limited to case series inMND and OHS. These reports usefully illustrate shared issuesin progressive NMD and many patients with advanced CWD.One report of outcome in MND following intubation forAHRF highlighted that 50% of patients were undiagnosed atthe time of intubation, only 17% weaned and few left hos-pital.216 Recently, Sancho et al217 reported a median survival of1 year in patients intubated after failing acute NIV. Chio et al214

reported on 1260 MND cases, over an 8-year period, from asingle Italian neurology centre; 134 patients received IMV,which was initiated as an emergency in 40%. Median survivalwas 250 days. Death occurred in hospital in 20%, at home in48% and in a nursing home in 32%. Neither patient experiencenor economic analysis was reported.

The outcome of patients with MND referred to a specialistweaning service in the UK was examined by Chadwick et al.218

Thirty patients had been transferred over a 15-year period.Diagnosis followed intubation in 17. In 14 patients, extubationto long-term NIV was possible, of whom 9 were non-bulbarcases and 10 returned home. Thirteen remained tracheostomyventilated, of whom 9 were bulbar and 7 returned home. Mediansurvival from tracheal intubation was 13.7 months (95% CI 0 to30.8) for those known to have MND and 7.2 months (95% CI5.1 to 9.4) for those not previously diagnosed.

There has been a call for the value of IMV in MND to bere-evaluated both as an elective policy and at the time of crisis.219

In many of the other NMDs, for example, acid maltase deficiencyand Duchene Muscular Dystrophy, a more prolonged survivalrate with a good QoL is to be expected following recovery fromAHRF, and an aggressive approach to managing it is, in theopinion of the guideline group, more justified than has historicallybeen the case in the UK. It is also what most patients and theirfamilies want. Expert experience is that the majority of patientswill survive a period of IMV. Comorbidity, especially associatedcardiomyopathy, is important prognostically. The weaning processis often prolonged but, in the absence of severe bulbar dysfuntion,many can be safely extubated onto NIVand avoid a tracheostomy.Should this fail, and a tracheostomy be required, specialist centreexperience is that subsequent decannulation is possible in most.While long-term survival may be limited, QoL may be acceptableand health status may improve with domicilary NIV. This is par-ticularly the case in the more slowly progressive NM conditionsand in stable CWD. In the latter group, even advanced pulmonaryhypertension may resolve.Evidence statementsThere are national (and centre) differences in use of IMV inAHRF complicating motor neurone disease (Level 3).The diagnosis of motor neurone disease, and other neuromuscu-lar conditions, is sometimes only made after admission to theICU for IMV (Level 3).De-cannulation of a tracheostomy is more difficult when there isbulbar disease (Level 3).Planned elective domiciliary NIV is preferable to crisismanagement in NMD and CWD. This reduces the risk of acutepresentation and provides a proven alternative to IMV whichrisks prolonged or permanent tracheostomy ventilation (Level 3).Recommendations54. In patients with NMD or CWD, senior staff should beinvolved in decision-making, in conjunction with home mechanicalventilation specialists, if experience is limited, and especially whenthe appropriateness of IMV is questioned (Grade D).

55. Advance care planning, particularly around the potentialfuture use of IMV, is recommended in patients with progressiveNMD or CWD. This may best be supported by elective referralto a home ventilation service (Grade D).

IMV strategy in NMD and CWDIn patients with NMD without significant chest wall distortion,the impedance to inflation is low. It is rarely necessary to use anIPAP above 20. It should initially be set at 10 and increasedaccording to the resulting tidal volume. In contrast, patientswith kyphoscoliosis usually require high inflation pressures.Expiration is generally not flow limited but impedence is typic-ally high so that an I:E ratio of 1 to 1 is recommended in bothdiagnostic groups.

When lung volume is reduced, there is radiological evidenceof lobar collapse or unexplained hypoxia, the PEEP setting onthe ventilator may need to be increased up to or above10 cm.14 15 Adjustments should be individualised according toventilatory parameters (RR, dynamic compliance, plateau pres-sure) and patient comfort.Good practice points▸ Patients with NMD usually require low levels of PS.▸ Patients with chest wall deformity usually require higher

levels of PS.▸ PEEP in the range 5–10 is commonly required to increase

residual volume and reduce oxygen dependency in bothpatient groups.

Obesity hypoventilation syndromeIn obese patients, hospitalised for any reason, the presence ofhypercapnia increases morbidity and mortality.220 Despite this,currently, there is a lack of evidence to guide treatment of eitherchronic hypercapnia or AHRF complicating obesity. One non-randomised trial suggested that long-term survival is better inthose who accept treatment for sleep disordered breathing com-pared with those who do not.221 Severe OSA is the principalcause of hypercapnia, but hypoventilation also results from themechanical effect of obesity.222

Presentation with acute on chronic respiratory failure is morecommon than de novo AHRF but the precipitant cause fordestabilisation may be unclear. Not uncommonly, chronic hyper-capnia is unexpectedly revealed peri-operatively followingroutine or emergency surgery in an obese patient not known tohave OHS. The possibility of OSA/OHS in the morbidly obese(BMI >35) needs to be borne in mind by surgical and anaes-thetic teams.

In the absence of evidence, we recommend that the indica-tions for NIV in the breathless obese patient should be the sameas in AECOPD ie pCO2 >6.5 and pH <7.35. Additionally, NIVshould be considered in any patient admitted to hospital with araised pCO2 who is excessively somnolent or when there is evi-dence of fluid retention. Following recovery, patients will needto be referred to an HMV centre. Patients with OHS can some-times be switched to CPAP at a later date.Evidence statementsIn patients with OHS, NIV is indicated if there is respiratoryacidosis using the same criteria as in AECOPD (Level 1–).In the absence of acidosis, NIV may be indicated in some hyper-capnic and/or somnolent obese patients (Level 2+).Recommendations56. Controlled oxygen therapy should be used in patients withOHS and AHRF (Grade D).57. In patients with OHS, NIV should be started in AHRF,using the same criteria as in AECOPD (Grade B).


BTS guidelines




58. NIV is indicated in some hospitalised obese hypercapnicpatients with daytime somnolence, sleep disordered breathingand/or right heart failure in the absence of acidosis (Grade D).

NIV settings and placement in OHSObese patients with severe AHRF have a significant risk,despite receiving NIV, of sudden deterioration and are likelyto be difficult to intubate (see below). Upper airway obstruc-tion is common and will be more apparent during sleep. Itmay persist, despite increasing the EPAP, as indicated by inter-mittent abdominothoracic paradox during NIV ‘assisted’breaths. Another clue is intermittent mask leak that accompan-ies obstructed inspiration. A more upright position may help,but an EPAP in the 10–15 range is often required. Expertassessment is recommended to titrate the EPAP. Tidal volumemay be compromised by high level EPAP and, in some, theimpedance to inflation is very high and an IPAP of >30 isrequired.217 Prolonging Ti will increase the resulting Vt deliv-ered so a I:E ratio of 1:1 is advised. If the resulting Vt is stillinadequate, consideration should be given to using volume-controlled ventilation or a volume-assured mode,92 althoughthe benefits of the latter are currently unproven. DifferentEPAP settings may be appropriate depending on sleep/awakestate.Good practice points▸ High IPAP and EPAP settings are commonly required in

patients with OHS (eg, IPAP >30, EPAP >8).▸ Volume control (or volume assured) modes of providing NIV

may be more effective when high inflation pressures arerequired.

NIV failure in OHSIn patients with OHS, the same indicators suggest a failingpatient and the same troubleshooting solutions apply as inAECOPD (see table 3). Fluid retention is common and itsextent is commonly under-estimated. It may be in excess of20 L. Achieving an SaO2 88–92% may be difficult and relates tocollapse of dependent lung and/or reflects underlying pulmon-ary vascular disease. Sudden and precipitous falls in oxygenationmay follow temporary removal of NIV. If high EPAP settings failto improve the A-a gradient, a ventilator offering oxygen blend-ing may be required. Difficulty in clearing secretions may con-tribute to poor gas exchange.Good practice points▸ Fluid overload commonly contributes to ventilatory failure in

patients with OHS and its degree is easily underestimated.▸ Forced diuresis may be useful.▸ As the risk of NIV failure is greater, and intubation may be

more difficult, placement in HDU/ICU for NIV isrecommended.

Discontinuing NIV in OHSDuring wakefulness, weaning of NIV should proceed as inAECOPD. NIV overnight should be continued pending discus-sion with the local home ventilation service. Other aspects, suchas consideration of bariatric surgery and optimal EPAP settingswhen returning home, are important aspects of continuing care.Good practice points▸ NIV can be discontinued as in patients with AECOPD.▸ Many patients with AHRF secondary to OHS will require

long-term domiciliary support (CPAP or NIV).▸ Following an episode of AHRF, referral to a home ventilation

service is recommended.

IMV strategy in OHSIntubation can be challenging and patient deterioration may berapid. There is also a higher risk of aspiration. Pressure controlis recommended until stability has been achieved and should beinitially set at 20 and increased according to the resulting tidalvolume. Inspiratory pressure in excess of 30 may be required.To recruit collapsed lung, PEEP may need to be 10–15 cm.14 15

It should be adjusted according to ventilatory parameters (RR,dynamic compliance, plateau pressure) and patient comfort.Good practice points▸ In patients with OHS, pressure-controlled MV is recom-

mended initially.▸ In patients with OHS, high PEEP settings may be needed to

recruit collapsed lung units and correct hypoxaemia.▸ In patients with OHS, forced diuresis is often indicated.

WEANING FROM IMVIntroductionWeaning is defined as the progressive reduction of ventilatorysupport leading up to extubation. Delayed weaning complicates6% of patients managed by IMV but consumes 37% of ICUresources.223 In one study, up to 50% of patients who self-extubated did not require re-intubation,224 implying that manypatients are treated with IMV for longer than necessary. Clinicalcriteria to be met before starting weaning are detailedbelow:225 226

▸ Adequate oxygenation: PaO2/FiO2 ratio >27 kPa (200 mmHg)▸ FiO2 <0.5▸ PEEP <10 cm H2O▸ Adequate alveolar ventilation (pH >7.3, pCO2 <6.5 kPa).

Fluid balance should also be optimised. The detrimentaleffect of excess hydration is now recognised in sepsis227 and inacute lung228 and kidney injury.229 A positive fluid balanceadversely affects alveolar ventilation, oxygenation, weaning pro-gress and extubation outcome.224 230 Brain Natriuretic Peptide(BNP) has been reported to predict failure to wean and corre-lates with weaning duration; a BNP-directed fluid managementstrategy has been reported to shorten time to extubation, par-ticularly in patients with left ventricular dysfunction.231

Evidence statementsEasily measured clinical parameters indicate when weaning canstart (Level 2+).Excess fluid administration may delay weaning or contribute toits failure (Level 2++).In left ventricular dysfunction, a BNP-directed fluid manage-ment strategy has been shown to shorten the duration of IMV(Level 2).Recommendations59. Treating the precipitant cause of AHRF, normalising pH,correcting chronic hypercapnia and addressing fluid overloadshould all occur before starting weaning (Grade D).60. A BNP-directed fluid management strategy should beconsidered in patients with known left ventricular dysfunction(Grade B).

Weaning methodsDespite several multinational studies, there is no consensus as tothe optimal weaning method. Brochard et al232 reported thatprogressively reducing PS was better than other weaningmethods. Subsequent trials have reported that daily (or multiple)T piece trials (SBTs) are as effective as PS weaning.233 234 It islikely that patient-specific characteristics are more importantthan the weaning protocol in determining the duration of


BTS guidelines




weaning. There is agreement that the Synchronised IntermittentMandatory Ventilation method is inferior to PS and T pieceweaning. It is also accepted that a formalised weaning plan, andstaff familiarity with the approach adopted on the ICU, areimportant factors to improve successful weaning.235

Evidence statementProgressive reduction of PS and daily SBTs are satisfactorymethods of weaning (Level 1+).Recommendations61. Assessment of the readiness for weaning should be under-taken daily (Grade B).62. A switch from controlled to assisted IMV should be made assoon as the patient recovery allows (Grade C).63. IMV patients should have a documented weaning plan(Grade B).

Assessing readiness for discontinuation of mechanicalventilationSBTs are used to assess readiness to resume normal breathing.During the SBT, a patient breathes with minimal or no PS(defined as <8). A successful trial requires the absence ofrespiratory distress. Failure of an SBT may be defined by subject-ive (comfort) or objective (deterioration in gas exchange or mea-sured ventilator parameters) criteria.232 233 Studies have shownthat the majority of SBT failures occur within 30 min.236 237

Repeated failure of SBT should lead to consideration of othermethods of weaning.238 239

It is important to note that the criteria that define success ofan SBT do not necessarily reflect the likelihood of successfulextubation. About 10% of patients who successfully manage anSBTwill fail to maintain adequate gas exchange and/or developsigns of distress following extubation.240 An SBT assesses thebalance of respiratory load to capacity of the respiratorymuscles but does not take into account other factors that mayaffect success such as upper airway patency, bulbar function,sputum load or effectiveness of cough.240

Evidence statementA SBT is useful in assessing load/capacity but does not predictthe success of extubation (Level 1+).Recommendation64. A 30 min SBT should be used to assess suitability for extuba-tion (Grade B).65. Factors including upper airway patency, bulbar function,sputum load and cough effectiveness should be considered priorto attempted extubation (Grade D).

Outcome following extubationSuccessful extubation is defined as the absence of the need forventilatory support for 48 h. Patients receiving post-extubationNIV (see below) are classified as ‘weaning in progress’.241

Much of the evidence regarding the prediction of the risk ofpost-extubation failure has come from trials of relatively shortduration IMV and with a mixture of underlying patholo-gies.235 242 243 Several risk factors have been identified.The more adverse factors present, the greater the risk ofextubation failure. Risk factors for extubation failure are shownin box 2.235 242 243

Respiratory distress may occur early or develop later on afterextubation. Early failure commonly results from loss of airwaypatency, for example, from upper airway oedema that becomesevident following removal of the endotracheal tube.244 Patientswith NMD are at risk of early extubation failure due to bulbardysfunction and/or ineffective cough despite a successful SBT.The planned use of NIV and an MI-E following extubation

reduces the risk of early failure. Late extubation failure is morecomplex in aetiology and more than one cause may be present.The causes are summarised below:244

▸ Capacity–load imbalance: patients with severe airflowobstruction or neuromuscular weakness;

▸ Impaired bulbar function: aspiration of upper airway secre-tions, impaired gas exchange and/or obstructed breathing;

▸ Ineffective cough: typically in NMD/CWD but also in otherpatients with AHRF;

▸ Non-respiratory issues—myocardial ischaemia/left ventriculardysfunction, encephalopathy/delirium or severe abdominaldistension.

Evidence statementPatient, clinical and ventilatory factors aid the identification ofpatients at increased risk of extubation failure (Level 2+).Recommendation66. Care is needed to identify factors that increase the risk ofextubation failure so that additional support, such as NIV orcough assist, can be provided (Grade B).

Weaning protocolsWeaning protocols that specify the steps to follow duringweaning have been claimed to reduce the duration of IMV,increase the success of extubation, reduce unplanned or acciden-tal extubation and reduce the tracheostomy rate, ventilator-associated complications and costs, compared with usualcare.245 The studies summarised in this review were, however,not specific to AHRF. Most were performed in the USA, wheredifferences in supervision of patient management exist com-pared with the UK. There is also marked variation in theweaning methods and protocols between the studies reported. AEuropean study reported that a weaning protocol did notreduce ventilation time.246 Computer-automated weaning, inwhich adjustment in pressure settings occurs in response tochanges in patient parameters, has been compared toprofessional-led weaning. One multicentre RCT found that dur-ation of weaning was reduced.247 A second study reported nodifference in weaning duration between automated weaning andweaning by an experienced nurse.248 There is currently insuffi-cient evidence to support the use of automated weaning overclinical/nurse-led protocols.Evidence statementsWeaning protocols may reduce the duration of IMV and ventila-tor associated pneumonia (Level 1+).

There is conflicting evidence regarding the value of computer-automated weaning (Level 1−).

Box 2 Risk factors for extubation failure followinginvasive mechanical ventilation (IMV)

▸ Positive fluid balance▸ Raised rapid shallow breathing index during spontaneous

breathing trial▸ Pneumonia or pulmonary disease as the cause requiring IMV▸ Increased age▸ Prolonged duration of IMV▸ Anaemia▸ Increased severity of illness▸ Low albumin▸ Previous failed extubation▸ Bulbar dysfunction


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Recommendations67. Although an organised and systematic approach to weaningis desirable, protocols should be used with caution in patientswith AHRF (Grade B).68. The use of computerised weaning cannot be recommendedin AHRF (Grade D).

Use of NIV in the ICUPlanned NIV to speed weaning from IMVIn an uncontrolled study on lung transplantation, NIV wasfound to speed extubation and reduce the time spent invasivelyventilated and the attendant complications.249 Subsequentstudies have compared the use of NIV with conventionalweaning in patients who have failed an SBT. Benefit was demon-strated in patients with underlying COPD.50 250 These studiesutilised NIV at high levels of PS and for longer than 24 h. NIVweaning was reported to confer no benefit in a subsequentstudy.251 A subsequent Cochrane review concluded that the useof NIV to speed weaning in patients with COPD reduced mor-tality and the incidence of pneumonia without increasing theneed for re-intubation.252

Evidence statementsNIV has been shown to accelerate weaning from IMV in thepatient with COPD failing an SBT (Level 1+).Recommendation69. NIV is recommended to aid weaning from IMV in patientswith AHRF secondary to COPD (Grade B).70. In other causes of AHRF, NIV may have a role in shorteningthe duration of IMV when local expertise in its use exists (andof cough assist when indicated) and there are features presentthat indicate extubation is likely to be successful (Grade D).

NIV in high-risk patientsNIV has been assessed in patients who have passed an SBT butwho have risk factors for extubation failure such as age>65 years, poor cough, cardiac and respiratory comorbidity,and hypercapnia (while ventilated and/or pre-existing). NIV wasreported to reduce the re-intubation rate and mortality in onestudy,253 and has been reported to be effective where obesity(BMI >35 kg/m2) is an additional adverse feature.254

Evidence statementsNIV may be effective in reducing respiratory failure,re-intubation and mortality in COPD (Level 1 +) and patientswith increased BMI (Level 2+).Planned post-extubation NIV reduces mortality, ICU and hos-pital length of stay and the incidence of ventilator-associatedpneumonia (Level 1−).Recommendation71. Prophylactic use of NIV should be considered to providepost-extubation support in patients with identified risk factorsfor extubation failure (Grade B).

NIV as ‘rescue’ therapy post-extubationA number of RCTs have examined the use of NIV as anunplanned ‘rescue’ treatment for post-extubation respiratory dis-tress. One multicentre RCT reported that patients who passedan SBT but who then developed post-extubation respiratoryfailure had an increased ICU mortality rate if treated with NIVas opposed to re-intubation.181 This study has been criticised asfew patients were treated in each participating centre, despite along recruitment period, raising the suspicion that lack of famil-iarity with NIV may have resulted in it being poorly applied.The patients who failed NIV and went on to require intubationalso received long periods of ineffective NIV before

re-intubation, 9 h longer than the control group. This may havecontributed to the worse outcome. Post hoc analysis suggested abenefit with NIV post-extubation in patients with COPD.Evidence statementThe use of NIV as rescue therapy for unexpected post-extubation respiratory failure does not improve outcome andmay be detrimental (Level 1+).Recommendations72. NIV should not be used routinely for unexpected post-extubation respiratory failure (Grade B).73. In COPD, a trial of NIV may be justified for unexpectedpost-extubation respiratory failure where local expertise exists(Grade D).

CARE PLANNING AND DELIVERY OF CAREAppropriate care environments for the delivery of NIVA study by Roessler and colleagues from Germany randomised51 patients to either out-of-hospital NIV or standard medicaltreatment. Out-of-hospital NIV was reported to be feasible, safeand effective.255 A survey of French mobile ICUs also suggeststhat NIV and CPAP can be safely employed pre-hospital in acutecardiogenic pulmonary oedema but not in other causes ofrespiratory failure.256 Further evaluation of out-of-hospital NIVin AHRF is required.

NIV is commonly initiated in the ED, but given the other pri-orities and pressures on emergency resuscitation areas patientsshould be transferred as soon as practicable to an environmentappropriately staffed and equipped to provide on going care. Aprospective observational study of 245 patients attending 24hospital EDs in Australia identified the staff responsible for NIVset-up.257 This was equally distributed between nursing andmedical personnel. Hess et al258 conducted a survey of 132 aca-demic EDs in the USA, and concluded that, although NIV waswidely available, physician confidence/competence was a barrierto optimal application. A survey of NIV use in UK EDs found awide variety of practice and suggested the need for a specificED guide for NIV.259 A pro forma-based COPD managementtool, supported by targeted education, was reported to improveED care including the use of NIV.260

Previous guidelines have recommended limiting the numberof areas providing NIV to ensure that staff perform it suffi-ciently regularly.48 Suitable sites need to be able to provide anNIV service 24/7 and integration with critical care services isessential. If NIV is provided in more than one area within a hos-pital, protocols and guidelines should be shared.261 CurrentNICE Quality Standards for COPD include guidance on how tobenchmark NIV provision.262 The requirements for an NIVservice are summarised in box 3.

For all but the mildest cases, Nava and Hill263 recommendthat NIV be delivered in a level 2 facility with enhanced staffinglevels. A survey carried out in 1999 found that NIV was pro-vided in level 2/3 facilities in most western European coun-tries.264 In contrast, NIV has been delivered in admission orrespiratory ward settings in the UK. This may partially accountfor the poor performance and high mortality rates associatedwith use of NIV reported by audits.3–5 The 2009 ICS recom-mendations265 reiterate level 2 as the appropriate clinical envir-onment for NIV and the 2008 joint BTS, ICS and RCP guideon the use of NIV in COPD with AHRF266 recommends onenurse for every 2 NIV cases, especially during the first 24 h oftreatment.

Despite this, in the 2013 BTS NIV audit, 91% of patientswere treated on general medical wards despite 43% havingpH<7.25.5 This was associated with a low intubation rate and


BTS guidelines




excess mortality. Although the care plan in 21% of casesincluded IMV should NIV fail, only 3% were intubated (versusan expected rate of 7%). Overall, the audit found that mortalityin the AECOPD group was 28% if NIV was delivered in HDU/ICU and 40% if not. With a median pH of 7.24 for the wholepatient population (2693 cases), this suggests that some werenot being treated for lesser degrees of acidosis, where NIVsuccess is more guaranteed, and that those receiving NIV werenot placed in the appropriate care environment given the sever-ity of acidosis.

A number of strategies have been explored to support theeffective use of NIV outside the HDU/ICU. Sala et al267

described the practicalities of creating a respiratory intermediatecare unit. Paus-Jenssen et al,268 in a Canadian prospective study,

used an expert respiratory therapist team to implement NIVacross a number of clinical environments. In a similar study, crit-ical care outreach nurses supported NIV delivery elsewhere inthe hospital. As a result, mortality was reduced from 57% to35%.183 A greater number of patients were also identified assuitable for IMV when failing NIV. Some of the challenges ofcare delivery in this field are highlighted in the National COPDAudit Programme 2014 findings on resources and organisationof care in acute National health Service (NHS) units,269 whereonly 30% of outreach programmes operated out of hoursduring weekdays and 59% of respiratory wards reported nolevel 2 capability. Cabrini reported an Italian prospective studyof NIV administered in a non-ICU setting but managed by ananaesthetist-led medical team.270 In 129 consecutive treatments,10% required intubation and there was a low mortality rate of12.4%. These reports together suggest that collaborationbetween admitting teams and the ICU can improve the deliveryof care in AHRF.

Hospitalisation with AHRF involves 3 phases—immediateclinical assessment, an assisted ventilation plan when appropri-ate and the formulation of a future care plan (short term in theevent of NIV failure and long term on recovery and dischargeor, depending on progress, the provision of end of life care).Figure 3 details key elements and box 4 provides a dischargechecklist.

It has been estimated that an average-sized district generalhospital, serving a population of 250 000, should anticipate,depending on local COPD prevalence, up to 100 AECOPDcases requiring ventilatory support per annum. Given the add-itional causes of AHRF, this probably equates to 150 NIV/IMVcases in most hospitals, and considerably more in areas withhigh COPD and/or OHS prevalence or those hospitals servinglarger populations. NIV facilities should be able to cope withseasonal variation and the increased demand that may occurduring influenza epidemics.271

Box 3 Essential requirements for an NIV service

▸ Specifically identified area(s) for NIV treatment at level 2equivalence.

▸ Staffing levels above that of a general medical ward withone nurse for every 2 NIV cases (especially during the first24 h of treatment)

▸ Locally developed NIV protocols (based on published bestpractice guides) uniformly applied across all areas

▸ A designated lead with a ‘core’ multidisciplinary group(physicians, nurses, physiotherapists) co-ordinating NIVservice provision and linked with critical care services

▸ Access to expert support for NIV technical advice in and outof hours

▸ Mechanisms for regular audit▸ Regular staff educational updates and training module for

new staff

Figure 3 The three phases of patient management in acute hypercapnic respiratory failure.


BTS guidelines




As discussed in the Management section, patient outcomesreported in UK national audits are notably worse than wouldbe expected from trial data and facilities for provision of NIV,and evidence of consultation with the ICU, are frequentlylimited or inadequate.3 4 7 Important deficiences that havebeen identified include delays in commencing ventilatorysupport, under-recognition of more complex acid–base distur-bances, use of inadequate ventilatory pressures, rare use of adifferent mask when NIV is failing, lack of progression fromNIV to IMV and lack of consultation in decision-making. Thepreponderance for application of NIV in lower level facilitiesthan elsewhere in the world (outlined above) along with evi-dence of a lack of integration with the ICU,3 4 indicates thatattention directed at organisational factors are needed and arehighly likely to improve patient outcome and experience inAHRF.

NIV facilities need to encompass adequate capacity, and theexpertise and associated staffing levels, to deal with complexcritically ill patients who have a significant risk of death. To beeffective, the NIV service needs to have good operational linksto the ICU in the expectation that 10% to 20% of NIV-treatedpatients should be managed in HDU/ICU and that many will bepotential candidates for IMV. The case for a specifically identi-fied and appropriately staffed and equipped area for providingNIV is strongly supported by the evidence. In some Europeancountries, NIV services are provided in a RespiratoryIntermediate Care Unit.264

Evidence statementsA care environment with either level 2 or 3 staffing favours asuccessful outcome from NIV therapy (Level 2+).Coordination between the ICU and ward areas improvesoutcome in AHRF (Level 3).Organisational aspects are pivotal in achieving best outcomes(Level 4).Recommendations74. NIV services should operate under a single clinical lead withformal working links with the ICU (Grade D).75. The severity of AHRF, and evidence of other organ dysfunc-tion, should influence the choice of care environment (Grade C) .76. NIV should take place in a clinical environment withenhanced nursing and monitoring facilities beyond those of ageneral medical ward (Grade C).

77. Initial care plans should should include robust arrangementsfor escalation, anticipating that up to 20% of AHRF cases shouldbe managed in a level 2 or 3 environment (Grade C).Good practice points▸ A 2–4 bedded designated NIV unit (located within a medical

high dependency area or within a respiratory ward withenhanced staffing levels) provides a robust basis for the provi-sion of NIV in a DGH serving a population of 250 000 andwith an average prevalence of COPD.

▸ Areas providing NIV should have a process for audit andinterdisciplinary communication.

Palliative care and advanced care planningIt is recognised that palliative interventions may be appropriateand yet be provided at the same time as therapies intended toprolong life.272 Accordingly, employing NIV as part of care thataims to relieve distress and has escalation limits may be entirelyjustified.

Effort is needed to establish patient preferences with respectto intubation or resuscitation status. Momen et al,273 in a sys-tematic review of end-of-life conversations in COPD, foundconsiderable variation among patients in the desire to discussend of life. Almost 50% of patients did not wish to have such aconversation and there was a preference to wait until the diseasewas ‘advanced’, with patient perception that this implied thelast few days of life. Advance directives/living wills assist health-care providers in tailoring clinical response and support.274 Theimportance of actively involving patient/family, especiallyregarding ‘do not attempt cardiopulmonary resuscitation’(DNACPR) orders, are highlighted in revised recommendationsfollowing a judicial ruling.275 The essential element is that,while patients cannot insist on CPR being performed, thematter should be discussed. Perceived patient ‘distress’—whichmight be exacerbated by such discussion—is no longer regardedsufficient grounds for not raising the issue. When the risk ofcausing physical or psychological harm is present, attemptsshould be made to talk to a healthcare advocate. The enormouschallenges in this serve to emphasise the crucial nature of activeand ongoing communication strategies. Chakrabarti reportedinterviews with 50 patients with stable COPD and found thatdiscussion and demonstration of NIV equipment altered futuretreatment perceptions and willingness to consider an advancedirective.276

Sinuff et al277 reported clinician attitudes to NIV in patientswith acute respiratory failure and do not intubate/do not resusci-tate instructions. While about 60% of physicians consideredthat NIV should be discussed in this context, 85% of respiratorytherapists (those actually administering NIV) felt NIV should beactively promoted. This may reflect a lack of confidence andunderstanding, among physicians, of the potential for NIV torelieve distress and be effective even in advanced disease. InDenmark, 15% of patients with do not intubate instructions,and who received NIV, survived at least a year with COPD andcongestive heart failure the most favourable underlyingdiagnoses.278

Evidence statementsIn advanced disease, care planning should ideally predate acutepresentation or commence as early as possible on presentationwith AHRF (Level 4).Health professionals experienced in NIV delivery have a morepositive view of the benefit of NIV and perceive patient treat-ment wishes more postively than do clinicians with less experi-ence of NIV (Level 4).

Box 4 Discharge checklist after AHRF

▸ Arrange early specialist review, pulmonary rehabilitation andhelp with smoking cessation as indicated.

▸ Consider early home visit, for example, outreach COPDteam/community nurses

▸ Discuss future care planning with patient/family and informcommunity services of the result of such discussion

▸ Provide warning card/inform ambulance services regardingfuture need for controlled oxygen therapy

▸ Consider referral to home NIV service, for example,neuromuscular disease (NMD) cases or suspected sleepdisordered breathing

▸ Review reasons/route of admission and consider methods toimprove if these were problematic

▸ Learn from any identified mistakes through multiprofessionalreview


BTS guidelines




Recommendations78. Clinicians delivering NIV or IMV should have ready accessto palliative medicine (Grade D).79. Multidisciplinary advance care planning should be an inte-gral part of the routine outpatient management of progressiveor advanced disease and care plans should be reviewed on pres-entation during an episode of AHRF (Grade D).80. The use of NIV may allow time to establish patient prefer-ence with regard to escalation to IMV (Grade D).

End-of-life careA questionnaire study of 118 patients with COPD, carried out inCanadian teaching hospitals,279 reported that patients withCOPD were less interested in prognosis, CPR, IMVor referral topalliative care than were patients with metastatic cancer. Inanother study, comparing QoL between patients with advancedCOPD and patients with cancer, patients with COPD reportedhigher levels of physical discomfort with uncontrolled shortnessof breath in 78%.280 A recent review of the 4 RCTs that haveexplored whether NIV relieves dyspnoea in AECOPD concludedthat benefit was likely but that study limitations constrained aconfident conclusion.281 With regard to physical symptoms,breathlessness and fatigue are dominant in AECOPD. Attentionto secretion clearance is an additional major concern in bronchi-ectasis and CF and for many with NMD. Ability to communicate,to feel safe, to be individually respected and enabled to retaincontrol are common psychological needs.

Patients receiving NIV as ‘ceiling care’, who fail to improvewill need appropriate end-of-life attention, including appropri-ate sedation/relief of distress. It is important that if withdrawalof NIV is decided on, that this is achieved with minimum dis-tress to the patient and their relatives. The BMA guidance onend-of-life care in 2007 did not address withdrawal of assistedventilation.282 Although withholding and withdrawing are con-sidered ethically equivalent,283 for many individuals, includingclinicians, discontinuing mechanical ventilation is felt be emo-tionally different to, for instance, stopping haemodialysis. Thismay be because of the immediacy of the consequence.284 AJapanese study reported interviews with 35 critical care physi-cians and found withdrawing ventilation was regarded differ-ently to stopping other life-sustaining measures because ofconcern over an abrupt and distressing demise.285 There was adesire for a ‘soft landing’, with a slow and gradual death per-ceived as ‘natural’. The ATS Clinical Policy Statement of 2007provides comprehensive guidance on withdrawal of mechanicalventilation, including symptom management of the dyingpatient. It emphasises that decision-making is a process requiringfrequent discussion with patient, family, health professionalsand others.286 Pro-active family-centred conferences allow timefor families to adjust and provision of literature on bereavementreduces the risk of subsequent emotional morbidity.287

In practical terms, progressive reduction of pressure/backuprate to achieve CO2 narcosis/coma and an alternative strategy ofextubation when intubated or removal of NIV have both beendescribed. In the former scenario, Cox et al288 suggest initialweaning of oxygen over 10 min with appropriate adjustment toopiate or anxiolytic medication. Once patient comfort isassured, it is suggested that mandatory ventilation is withdrawnand PS reduced to zero over 5–10 min. Kuhnlein et al289 con-ducted structured interviews with 29 families regarding the cir-cumstances of dying in MND patients receiving NIV. Seventeencaregivers described the final stages and eventual death as‘peaceful’. Eleven of the patients died peacefully while usingNIV. Choking sensation was evident in some bulbar patients.

The authors indicated that the use of sedatives, anxiolytics andopiates could have been improved, emphasising that palliativecare training or support is needed to achieve best practice.

In conclusion, the role of NIV in achieving a ‘good death’may currently be underutilised and there may be a lack ofappreciation that a peaceful death can occur while receiving sup-portive ventilation.Evidence statementsThe concerns of patients with COPD towards their end of life,centre on high levels of physical symptoms, especially breath-lessness (Level 3).Clinicians often consider withdrawal of assisted ventilation(NIV/IMV) as more challenging than removal of other lifesupport techniques (Level 4).Good practice points▸ Although removal of the NIV mask may be deemed as pref-

erable, a dignified and comfortable death is possible with itin place.

▸ Clinicians delivering NIV or IMV should have training inend-of-life care and the support of palliative care teams.

NOVEL THERAPIESExtracorporeal CO2 removalThe technical aspects of providing prolonged extracorporealmembrane oxygenation (ECMO) or CO2 removal (ECCO2R)have advanced in recent years. Both are being increasingly inves-tigated in refractory respiratory failure including AHRF. NICEhas issued general guidance on the use of ECCO2R advisingthat it should only be used in patients with potentially reversiblehypercapnic respiratory failure or those being considered forlung transplantation.290

ECCO2R uses a gas exchange membrane to provide partialCO2 clearance, from 30% to 50% of the body’s production,depending on blood flow and membrane efficiency. Removingcarbon dioxide extracorporeally reduces the native pulmonaryminute ventilation required to maintain an acceptable PaCO2.This offers the potential benefits of either enabling protectivemechanical ventilation or providing an alternative to mechanicalventilation in selected patients (such as those with COPD).There is little evidence of clear benefits to patients of ECCO2Rat present. In moderately hypoxaemic ARDS, one RCT demon-strated that lower tidal volumes and ventilatory pressures couldbe achieved, but this failed to translate into a meaningfulimprovement in patient outcome.291 Larger studies are plannedin the UK and Europe. In patients with COPD, there are noRCTs exploring the role of ECCO2R. One retrospectivelymatched cohort study compared outcomes between groups ofpatients with AECOPD who had an inadequate response to NIV.Twenty five potential candidates who had failed to improve withNIV were compared with historical controls treated in the samehospitals matched by the GenMatch process. Despite significantimprovements in acidosis and respiratory distress, the trial failedto show benefit in the primary outcome of need for intubation.The complication rate with ECCO2R was high (52%) and thiscontributed to the need for intubation.292

The devices available for ECCO2R have evolved over time.Early CO2 removal membranes were pumpless, required arterialand venous cannulation and used the patients own cardiacoutput to drive blood through the membrane. This resulted insignificant shunting of cardiac output and the danger of limbischaemia. An alternative approach is to take blood from a dual-lumen large bore cannula sited in a central vein and pump itthrough the membrane. The advantages of the veno-venous


BTS guidelines




technique are principally lack of effect on cardiac output andreduced complications, particularly limb ischaemia.Evidence statementsExtra-corporeal CO2 removal devices can reduce PaCO2 andminute volume (Level 2−).Veno-venous extra-corporeal CO2 removal in patients withAECOPD and an inadequate response to NIV has not beenshown to reduce intubation rate and is associated with a 52%complication rate (Level 2−).Recommendations81. If local expertise exists, ECCO2R might be considered:▸ If, despite attempts to optimise IMV using lung protective

strategies, severe hypercapnic acidosis (pH <7.15) persists(Grade D);

▸ When ‘lung protective ventilation’ is needed but hypercapniais contraindicated, for example, in patients with coexistentbrain injury (Grade D);

▸ For IMV patients awaiting a lung transplant (Grade D).Good practice pointECCO2R is an experimental therapy and should only be usedby specialist intensive care teams trained in its use and whereadditional governance arrangements are in place or in thesetting of a research trial.

Helium/oxygen ventilationWhen mixed with oxygen (Heliox), the lower density of heliumreduces resistance in the large airways where flow is predomin-antly turbulent compared to air/oxygen ventilation. It thereforehas a theoretical advantage in obstructive causes of AHRF.293

Heliox has been studied in combination with both NIV andIMV. It increases the delivered dose of bronchodilators and hasbeen reported to improve symptoms and physiological variablesin spontaneously breathing asthmatics.294 295 At oxygen concen-trations >40%, Heliox has no benefit compared with oxygen–air mixtures.296 A large RCT in AECOPD found that Heliox incombination with NIV did not reduce rates of intubation, dur-ation of ventilatory support or mortality.297 Heliox has beenreported to reduce pCO2 and airway pressures in intubatedpatients with severe asthma298 but a subsequent meta-analysisconcluded that it did not affect outcome.299 An uncontrolledstudy reported that Heliox improved patient comfort in thepresence of post-extubation respiratory distress when stridorwas present.300

Evidence statementThe use of Heliox does not reduce rates of intubation andlength of IMV, nor does it reduce mortality in patients ofAECOPD or asthma (Level 1+).Recommendation82. Heliox should not be used routinely in the management ofAHRF (Grade B).

Author affiliations1British Thoracic Society, London, UK2St James’s University Hospital, Leeds, UK3Barts Health NHS Trust, London, UK4Department of Respiratory Research, University Hospitals of Coventry andWarwickshire NHS Trust, Coventry, UK5Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK6Department of Respiratory, Scottish Pulmonary Vascular Unit, Glasgow, UK7Royal Surrey County Hospital NHS Foundation Trust and Faculty of Health andMedical Sciences, University of Surrey, Guildford, UK8Academic Respiratory Unit, University of Bristol, Bristol, UK9North Bristol Lung Centre, North Bristol NHS Trust, Bristol, UK10University Hospital of South Manchester NHS Foundation Trust, Manchester, UK11Emergency Department, Manchester Royal Infirmary, Central Manchester UniversityHospitals NHS Foundation Trust, Manchester, Manchester, UK M13 9WL

12University of Plymouth, Plymouth, UK13Department of Physiotherapy, Guy’s and St Thomas’ NHS Foundation Trust, StThomas’ Hospital, London, UK14Aintree University Hospital, Liverpool, UK15CLAHRC, Imperial College, London, UK16Queen’s Medical Centre, Nottingham, UK17Royal College of Physicians, London, UK

Twitter Follow BTS at @BTSrespiratory, Ben Creagh-Brown at @SPACeRGroup andJames Dodd at @theotherdodd

Acknowledgements The authors acknowledge assistance with developing theaims and structure of the guidelines provided by Martin Wildman, Simon Baudouin,Robert Winter, Sara Bolton, Mandy Odell, David Smith and the members of the BTSStandards of Care Committee.

Collaborators BTS Standards of Care Committee members: Colin Gelder, JamesDodd and Caroline Patterson.

Contributors ACD chaired the guideline group, and led the drafting and revisionof the document. He has final responsibility for the guideline. SB, ME, DK, CG andAG drafted and revised the paper. CC, BC-B, JD, TF, BF, LM, LMcD, RP, CP, MS andLT conducted appraisal of the literature and provided draft sections of the document.

Representation Dr Bob Winter and Sara Bolton represented the Intensive CareSociety, Dr Bernard Foëx represented the College of Emergency Medicine, Dr DanielKennedy represented the Royal College of Anaesthetists and Surgeon Captain LynnThomas represented the Royal College of Physicians.

Competing interests ACD declares being paid as a consultant to Smith Medicalbetween 2008 and 2013. ME declares he has received an honorarium, and traveland subsistence expenses for speaking at a meeting in Australia organised byResmed, a Respiratory Sleep and Ventilation company. He has received anhonorarium and travel expenses for speaking at a meeting in London organised byPhillips Respironics, a Respiratory Sleep and Ventilation company. He has receivedtravel and subsistence expenses for speaking at a meeting in China organised byCurative Medical Inc, a Respiratory Sleep and Ventilation company. He has receivedtravel expenses for speaking at meetings in India organised by Phillips Respironics, aRespiratory Sleep and Ventilation company. AG declares being paid as a consultantand receiving honoraria and travel expenses for speaking at meetings organised byArmstrong Medical Ltd in the UK, between 2014 and 2015.

Provenance and peer review Not commissioned; internally peer reviewed.

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http://twitter.com/theotherdodd

http://dx.doi.org/10.1136/thorax.57.3.192


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http://dx.doi.org/10.1136/thx.2010.153114

http://dx.doi.org/10.1186/cc2835


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http://dx.doi.org/10.1007/s00134-001-1146-9

http://dx.doi.org/10.1007/s00134-002-1421-4

http://dx.doi.org/10.1378/chest.127.5.1784

http://dx.doi.org/10.1007/s00134-010-1994-2

http://dx.doi.org/10.1007/s00134-010-1994-2

http://dx.doi.org/10.1007/s00134-011-2416-9

http://dx.doi.org/10.1007/s00134-011-2416-9

http://dx.doi.org/10.1378/chest.08-3018


http://dx.doi.org/10.1007/s00134-008-1327-x

http://dx.doi.org/10.1007/s00134-010-2066-3

http://dx.doi.org/10.1097/CCM.0b013e31819b575f

http://dx.doi.org/10.1590/S1806-37132009000200010

http://dx.doi.org/10.1590/S1806-37132009000200010

http://dx.doi.org/10.1097/00003246-200006000-00015

http://dx.doi.org/10.1213/ane.0b013e3181a1f708

http://dx.doi.org/10.1183/09031936.04.00051604

http://dx.doi.org/10.1007/s00134-002-1208-7

http://dx.doi.org/10.1097/01.CCM.0000045563.64187.20

http://dx.doi.org/10.1097/CCM.0b013e31819fff93

http://dx.doi.org/10.1097/00000542-200401000-00007

http://dx.doi.org/10.1007/s00134-003-1825-9

http://dx.doi.org/10.1007/s00134-006-0391-3

http://dx.doi.org/10.1007/s00134-006-0391-3

http://dx.doi.org/10.1097/01.mej.0000072627.17469.43

http://dx.doi.org/10.1097/01.mej.0000072627.17469.43

http://dx.doi.org/10.1007/BF03040454

http://dx.doi.org/10.1007/s00134-003-1925-6

http://dx.doi.org/10.1111/j.1399-6576.2007.01474.x

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http://dx.doi.org/10.1016/0009-8981(61)90032-8

http://dx.doi.org/10.1016/0009-8981(61)90032-8


http://dx.doi.org/10.1007/s00134-010-2076-1

http://dx.doi.org/10.4103/1817-1737.84776

http://dx.doi.org/10.4187/respcare.03335

http://dx.doi.org/10.1136/thx.47.1.34

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BTS guidelines


http://dx.doi.org/10.1016/j.jcrc.2008.12.009

http://dx.doi.org/10.1111/j.2042-7158.2010.01134.x

http://dx.doi.org/10.1097/01.CCM.0000284512.21942.F8

http://dx.doi.org/10.1007/s00134-010-1904-7

http://dx.doi.org/10.1213/ane.0b013e3181732dc2

http://dx.doi.org/10.1007/s00134-006-0447-4

http://dx.doi.org/10.1007/s00134-006-0447-4

http://dx.doi.org/10.1007/s00134-010-2026-y

http://dx.doi.org/10.1016/j.curtheres.2010.06.003


http://dx.doi.org/10.1186/2049-6958-9-56

http://www.aomrc.org.uk/doc_details/9737-safe-sedation-practice-for-healthcare-procedures-standards-and-guidance











http://dx.doi.org/10.1093/bja/aet070

http://dx.doi.org/10.1183/09031936.03.00048102




http://dx.doi.org/10.1016/S0272-5231(03)00046-7

http://dx.doi.org/10.4103/1817-1737.94531


http://dx.doi.org/10.1097/CCM.0b013e3181bc8243



http://dx.doi.org/10.1097/CCM.0b013e318170f0f3

http://dx.doi.org/10.1007/s001340050688

http://dx.doi.org/10.1097/CCM.0b013e3181c587fd

http://dx.doi.org/10.1164/ajrccm/136.4.872


http://dx.doi.org/10.1001/jama.282.1.54

http://dx.doi.org/10.1056/NEJM200005043421801



http://dx.doi.org/10.1007/s001340050772

http://dx.doi.org/10.1183/09031936.98.12061242

http://dx.doi.org/10.1002/14651858.CD002881

http://dx.doi.org/10.1007/s00134-004-2255-z

http://dx.doi.org/10.1007/s00134-002-1438-8



http://dx.doi.org/10.1183/09031936.97.10071663







http://dx.doi.org/10.1007/BF01712327

http://dx.doi.org/10.1007/s001340051339

http://dx.doi.org/10.1592/phco.27.3.389

http://dx.doi.org/10.1097/00003246-199805000-00034

http://dx.doi.org/10.1097/CCM.0b013e3182783b72

http://dx.doi.org/10.1097/CCM.0b013e3182783b72




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BTS guidelines


http://dx.doi.org/10.1016/S0140-6736(08)60105-1

http://dx.doi.org/10.1097/00003246-199912000-00001

http://dx.doi.org/10.1097/CCM.0b013e31817bfd60

http://dx.doi.org/10.1164/rccm.201102-0273CI

http://dx.doi.org/10.1097/CCM.0b013e3182a168c5

http://dx.doi.org/10.1001/jama.2012.13872


http://dx.doi.org/10.1097/CCM.0b013e3181a98a05


http://dx.doi.org/10.1097/CCM.0b013e318225753c

http://dx.doi.org/10.1007/s00134-009-1467-7

http://dx.doi.org/10.1007/s00134-002-1311-9

http://dx.doi.org/10.1097/00003246-199710000-00016

http://dx.doi.org/10.1007/s00134-006-0301-8

http://dx.doi.org/72897

http://dx.doi.org/10.1097/01.CCM.0000260055.64235.7C

http://dx.doi.org/10.1007/s00134-011-2297-y

http://dx.doi.org/10.1007/s00134-008-1209-2

http://dx.doi.org/10.1097/CCM.0b013e3181cb0d7b

http://dx.doi.org/10.1007/s00134-010-2052-9

http://dx.doi.org/10.1097/CCM.0b013e31818444a5

http://dx.doi.org/10.1097/01.CCM.0000134835.05161.B6

http://dx.doi.org/10.1136/bmj.38467.485671.E0

http://dx.doi.org/10.1111/j.1365-2044.2004.04106.x




http://dx.doi.org/10.1093/bja/aeq238

http://dx.doi.org/10.1097/01.CCM.0000229882.09677.FD

http://dx.doi.org/10.1097/01.CCM.0000229882.09677.FD

http://dx.doi.org/10.1093/bja/aer059

http://dx.doi.org/10.1093/qjmed/hci084

http://dx.doi.org/10.1007/s00134-005-0050-0

http://dx.doi.org/10.1007/s00134-002-1478-0


http://dx.doi.org/10.1164/rccm.201106-1094OC

http://dx.doi.org/10.1164/rccm.201111-1933ED

http://dx.doi.org/10.1164/rccm.201111-1933ED

http://dx.doi.org/10.1016/S0140-6736(00)02323-0




http://dx.doi.org/10.1093/ageing/afr003

http://dx.doi.org/10.1111/j.1742-1241.2012.02904.x


http://dx.doi.org/10.1183/09031936.05.00085304

http://dx.doi.org/10.1001/jama.287.24.3238

http://dx.doi.org/10.1136/bmj.326.7382.185






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BTS guidelines


http://dx.doi.org/10.1007/s00134-005-2582-8

http://dx.doi.org/10.1056/NEJMoa032736

http://dx.doi.org/10.1136/bmj.39371.524271.55

http://dx.doi.org/10.1016/j.iccn.2011.04.002



http://dx.doi.org/10.1016/j.ejim.2007.04.017

http://dx.doi.org/10.1046/j.1525-1497.2003.20615.x


http://dx.doi.org/10.1183/09031936.96.09030422


http://dx.doi.org/10.1111/j.1440-1843.2010.01795.x



http://dx.doi.org/10.1080/02770900902718829

http://dx.doi.org/10.1111/j.1553-2712.2001.tb01128.x

http://dx.doi.org/10.1111/j.1553-2712.2001.tb01128.x

http://dx.doi.org/10.2169/internalmedicine.47.0429


http://dx.doi.org/10.1002/14651858.CD004360.pub4



http://dx.doi.org/10.1007/s00134-009-1743-6

http://dx.doi.org/10.1016/j.hrtlng.2009.06.014

http://dx.doi.org/10.1007/s00134-006-0085-x

http://dx.doi.org/10.4021/jocmr612w

http://dx.doi.org/10.1016/j.jcf.2003.12.003

http://dx.doi.org/10.1183/09031936.02.00218502

http://dx.doi.org/10.1186/1465-9921-7-14

http://dx.doi.org/10.1111/resp.12051




http://dx.doi.org/10.1016/S1474-4422(05)70326-4

http://dx.doi.org/10.1136/jnnp.2009.175984

http://dx.doi.org/10.1136/jnnp.72.6.752





http://dx.doi.org/10.1016/j.amjmed.2003.08.022


http://dx.doi.org/10.1053/rmed.1999.0732

http://dx.doi.org/10.1164/ajrccm/140.2_Pt_2.S14


http://dx.doi.org/10.1164/rccm.2206020

http://dx.doi.org/10.1097/01.CCM.0000194725.48928.3A



http://dx.doi.org/10.1007/s00134-005-2801-3








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238 Ely EW, Baker AM, Dunagan DP, et al. Effect on the duration of mechanicalventilation of identifying patients capable of breathing spontaneously. N Engl JMed 1996;335:1864–9.

239 Vallverdu I, Calaf N, Subirana M, et al. Clinical characteristics, respiratoryfunctional parameters, and outcome of a two-hour T-piece trial in patientsweaning from mechanical ventilation. Am J Respir Crit Care Med1998;158:1855–62.

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BTS guidelines



http://dx.doi.org/10.1007/s00134-002-1353-z




http://dx.doi.org/10.1007/s00134-002-1268-8

http://dx.doi.org/10.1183/09031936.00010206

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http://dx.doi.org/10.1007/s00134-004-2231-7

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https://www.nice.org.uk/guidance/qs10

http://dx.doi.org/10.1016/S0140-6736(09)60496-7

http://dx.doi.org/10.1183/09031936.02.00058202

https://www.brit-thoracic.org.uk/guidelines-and-quality-standards/non-invasive-ventilation-(niv)/

https://www.brit-thoracic.org.uk/guidelines-and-quality-standards/non-invasive-ventilation-(niv)/

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APPENDIX 1 GUIDELINE GROUP MEMBERSChair: Craig DavidsonWriting GroupsAcute NIVGroup lead: Mark Elliott,Members: Colin Church, Tim Felton, Milind Sovani, LynnMcDonnellInvasive Mechanical VentilationGroup lead: Daniel KennedyMembers: Ben Creagh-Brown, Craig Davidson, AlastairGlossop, Leigh Mansfield,Care PlanningGroup lead: Steve BanhamMembers: Rob Parker, Craig Davidson, Ben Creagh-Brown,Lynn Thomas, Bernard Foëx


BTS guidelines




http://dx.doi.org/10.1097/CCM.0b013e3181b78abe


http://dx.doi.org/10.1111/j.1365-2044.2006.04897.x





respiratory failure in adultsmanagement of acute hypercapnic BTS/ICS guideline for the ventilatory

Standards of Care CommitteeGuideline Development Group, On behalf of the British Thoracic SocietySociety/Intensive Care Society Acute Hypercapnic Respiratory Failure Thomas and BTS Standards of Care Committee Member, British ThoracicMcDonnell, Robert Parker, Caroline Marie Patterson, Milind Sovani, Lynn James William Dodd, Tim Felton, Bernard Foëx, Leigh Mansfield, LynnGelder, Alastair Glossop, Alistair Colin Church, Ben Creagh-Brown, A Craig Davidson, Stephen Banham, Mark Elliott, Daniel Kennedy, Colin

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Correction

Davidson AC, Banham S, Elliott M, et al. BTS/ICS guideline for the ventilatory managementof acute hypercapnic respiratory failure in adults. Thorax 2016;71 Suppl 2:ii1–35. doi:10.1136/thoraxjnl-2015–208209.

The British Thoracic Society wishes to clarify reference to the definition of hypercapnia inrelation to the BTS/ICS Guidelines for the ventilatory management of acute hypercapnicrespiratory failure (2016).

The British Thoracic Society recognises the definition of hypercapnia as a PaCO2 ≥6 kPa asused in the BTS Standards of Care document on non invasive ventilation in acute respiratoryfailure1 and BTS Guidelines for Emergency Oxygen Use in Adults.62

Previous guidelines recommended that NIV be considered if pH <7.35 and PaCO2 >6 kPaand RR >23 breaths/min. These were predominantly written for patients with exacerbationsof Chronic Obstructive Pulmonary Disease.48 NIV use in the UK has since broadened to treata number of other diagnoses where the evidence for benefit is less robust and where some-times there is a mixed metabolic and respiratory acidosis.

In the 2016 BTS/ICS Guidelines for the ventilatory management of acute hypercapnicrespiratory failure, the guideline development group considered that in patients with type 2respiratory failure, a PaCO2 between 6.0 and 6.5 kPa is unlikely to make a large contributionto acidosis. Consensus within the guideline development group and open consultation on thedraft guidelines suggested that these patients should receive optimal medical care and con-trolled flow oxygen while NIV is considered.

The convention and guidance in many centres has evolved to limit the widespread use ofNIV in acidosis with a large metabolic contribution and to initiate NIV only in those patientswhere repeat arterial blood gas measurement confirms a persisting respiratory acidosis pH<7.35 with a higher threshold for PaCO2 >6.5 kPa.

The BTS/ICS Guidelines for the ventilatory management of acute hypercapnic respiratoryfailure recommendation 25 is amended to:

NIV should be started when a pH <7.35, a PaCO2 of ≥6.5 kPa and RR >23 breaths/minspersists or develops after an hour of optimal medical therapy. (Grade A)

For patients with a PaCO2 between 6.0 and 6.5 kPa NIV should be considered.(Grade D).

The following corrections are also noted:

Page 6 - Definition of AHRF:“Conventionally a pH <7.35 and a PCO2 >6.0kPa confirms acute respiratory acidosis

and, when persisting after initial medical therapy, have been used as threshold values for con-sidering the use of non-invasive ventilation.”

Page 16:“In around 20% of AHRF cases secondary to AECOPD, optimised medical therapy, which

includes targeting an oxygen saturation to 88–92%, will result in normalisation of arterialpH.2 62 Established guidance is to await improvement and initiate NIV if, after 60 min, thefollowing are present: pH <7.35, pCO2 >6.0 kPa and RR >23 breaths/min.1 48

REFERENCES1 British Thoracic Society Standards of Care Committee. Non-invasive ventilation in acute respiratory failure. Thorax

2002;57:192–211.2 Plant PK, Owen J, Elliott MW. One year period prevalence study of respiratory acidosis in acute exacerbation of COPD;

implications for the provision of non-invasive ventilation and oxygen administration. Thorax 2000;55:550–4.48 NICE clinical guidance [CG12]. Chronic obstructive pulmonary disease - Management of chronic obstructive pulmonary disease

in adults in primary and secondary care. 2004. http://www.nice.org.uk/guidance/cg1262 O’Driscoll BR, Howard LS, Davison AG, et al. BTS guideline for emergency oxygen use in adult patients. Thorax 2008;63:

(Suppl_6):vi1–68.

588 Thorax June 2017 Vol 72 No 6

PostScript

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